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Aim: The aim of this observational study was to determine the immune status and function in young adults with cerebral palsy (CP) in comparison to typically developing individuals. Method: Blood samples from 12 individuals with CP (five males, seven females; mean age: 25 years 1 month (5 years 9 months); age range: 19–38 years) and 17 typically developing individuals (eight males, nine females; mean age: 31 years 4 months (6 years 2 months); age range: 20–40 years) were collected before, immediately after, and 1 hour after 45 minutes of frame running or running respectively. Independent t‐tests were used to compare heart rate, level of exertion, and baseline cell proportions between groups. Mixed model analysis of variance was utilized to investigate immune cell responses to exercise across groups. Results: Baseline levels of gamma delta (TCRγδ+) T‐cells were significantly higher (absolute percentage: +2.65, p = 0.028) in the individuals with CP. Several cell populations showed similar significant changes after exercise in both CP and typically developing groups. Cytotoxic (CD8+) T‐cells were only significantly elevated immediately after exercise in the typically developing participants (p < 0.01). Individuals with CP exhibited significantly lower heart rates (−11.1%, p < 0.01), despite similar ratings of perceived exertion. Interpretation: Elevated baseline TCRγδ+ T‐cells may indicate low‐grade inflammation in adults with CP. Although most of the cell populations showed typical responses to endurance exercise, the absence of response in CD8+ T‐cells in individuals with CP may indicate the need for higher intensity during exercise. What this paper adds: TCRγδ+ T‐cell baseline levels are elevated in adults with cerebral palsy (CP).The CD8+ T‐cell response to exercise was blunted in adults with CP.Exercise intensity is decisive for CD8+ T‐cell responses in individuals with CP. [ABSTRACT FROM AUTHOR]

Evidence of cognition in aneural cells is well‐establish in the literature. This paper extends the exploration of the mechanisms of cognition by considering whether or not aneural cells may be capable of irrational cognition, making associations based on coincidental similarities and circumstantial factors. If aneural cells do harness such semiosic qualities, as with higher‐level creativity, this might be how they are able to overcome old algorithms and invent tools for new situations. I will look at three examples of irrational learning in aneural systems in terms of semiotics: (1) generalisation in the immune system, based on viral molecular mimicry, whereby immune cells attack the self, which seems to be an overgeneralisation of an icon sign based on mere similarity, not identity, (2) the classical conditioning of pea plants to trope toward wind as a sign of light, which seems to be an association of an index sign based on mere temporal proximity, and (3) a pharmaceutical intervention to prevent pregnancy, using a conjugate to encrypt self with non‐self, which seems to be an example of symbol use. We identify irrational cognition easily when it leads to 'wrong' outcomes, but, if it occurs, it may also lead to favourable outcomes and 'creative' solutions. [ABSTRACT FROM AUTHOR]

Irritable bowel syndrome (IBS), one of the most prevalent functional gastrointestinal disorders, is characterized by recurrent abdominal pain and abnormal defecation habits, resulting in a severe healthcare burden worldwide. The pathophysiological mechanisms of IBS are multi‐factorially involved, including food antigens, visceral hypersensitivity reactions, and the brain–gut axis. Numerous studies have found that gut microbiota and intestinal mucosal immunity play an important role in the development of IBS in crosstalk with multiple mechanisms. Therefore, based on existing evidence, this paper elaborates that the damage and activation of intestinal mucosal immunity and the disturbance of gut microbiota are closely related to the progression of IBS. Combined with the application prospect, it also provides references for further in‐depth exploration and clinical practice. [ABSTRACT FROM AUTHOR]

Depression is a serious public health problem, and adolescence is an 'age of risk' for the onset of Major Depressive Disorder. Recently, we and others have proposed neuroimmune network models that highlight bidirectional communication between the brain and the immune system in both mental and physical health, including depression. These models draw on research indicating that the cellular actors (particularly monocytes) and signaling molecules (particularly cytokines) that orchestrate inflammation in the periphery can directly modulate the structure and function of the brain. In the brain, inflammatory activity heightens sensitivity to threats in the cortico‐amygdala circuit, lowers sensitivity to rewards in the cortico‐striatal circuit, and alters executive control and emotion regulation in the prefrontal cortex. When dysregulated, and particularly under conditions of chronic stress, inflammation can generate feelings of dysphoria, distress, and anhedonia. This is proposed to initiate unhealthy, self‐medicating behaviors (e.g. substance use, poor diet) to manage the dysphoria, which further heighten inflammation. Over time, dysregulation in these brain circuits and the inflammatory response may compound each other to form a positive feedback loop, whereby dysregulation in one organ system exacerbates the other. We and others suggest that this neuroimmune dysregulation is a dynamic joint vulnerability for depression, particularly during adolescence. We have three goals for the present paper. First, we extend neuroimmune network models of mental and physical health to generate a developmental framework of risk for the onset of depression during adolescence. Second, we examine how a neuroimmune network perspective can help explain the high rates of comorbidity between depression and other psychiatric disorders across development, and multimorbidity between depression and stress‐related medical illnesses. Finally, we consider how identifying neuroimmune pathways to depression can facilitate a 'next generation' of behavioral and biological interventions that target neuroimmune signaling to treat, and ideally prevent, depression in youth and adolescents. [ABSTRACT FROM AUTHOR]

Major studies are still lacking on the impact of differing intensities of long-term donor plasmapheresis, not only on total serum protein, albumin and immunoglobulin G (IgG), but also on humoral and cellular immunity, red cell and iron metabolism, and biochemical cardiovascular risk markers. Three groups of donors, comprising 483 individuals undergoing differing intensities of long-term serial plasmapheresis, were entered into a cross-sectional study. A fourth control group consisted of 100 non-donors. In addition to measuring total protein, albumin and IgG levels, we determined parameters of humoral and cellular immunity, red cell and iron metabolism and recognized biochemical cardiovascular risk factors. The median annual net amount of plasma donated by the three donor groups was 37, 16 and 10 l, respectively ( P < 0·0001). Donors had significantly lower total serum protein, albumin and IgG levels than non-donors ( P < 0·0001), but the intensity of plasmapheresis had no influence on those parameters. Like non-donors, all plasma donors had normal humoral and cellular immunity. No increased rates of iron store depletion were observed in the three groups of plasma donors. Plasma donors were not at increased cardiovascular risk. Regular donor plasmapheresis of up to 45 l of plasma per year appears to be as safe as more moderate plasmapheresis programmes, with respect to the parameters analysed in this study. Individuals donating under these conditions did not develop impaired humoral and cellular immunity, iron store depletion, or increased cardiovascular risk with regard to established biochemical risk markers. Prospective studies are required to determine more exactly than in retrospective analyses the reasons why donors withdraw from plasmapheresis programmes. [ABSTRACT FROM AUTHOR]

The 48 G>C transversion in exon 1 of the RHCE gene leads to Trp16Cys, usually present in the conventional RHCE Ce, while Trp16 is associated with RHCE ce. The presence of Cys16 in RHCE ce is associated with the R0 (Dce) haplotype in Africans, leading to a weak ‘e’ antigen expression on red blood cells (RBCs). VS is a common red cell antigen in individuals of African descent and results from a single point mutation in exon 5 of the RHCE (733C>G), leading to Leu245Val substitution; VS positivity is also associated with weak expression of ‘e’. This study investigated the association of Cys16 and/or VS with the RHCE ce alleles in a cohort of sickle cell disease (SCD) patients phenotyped as R0r or R0R0 and rr. DNA samples from 58 SCD patients were tested for the 48 G>C transversion, encoding Cys16, by allele-specific polymerase chain reaction (PCR). We also amplified exon 5 of the RHCE by PCR and subjected the amplified product to restriction fragment length polymorphism analysis, using BfaI, in order to determine the VS status. Further cDNA analysis was performed on three samples to verify whether the mutations were located on the same or on different alleles. Fifty-six of the 58 SCD patients studied (97%) were heterozygous for 48G/48C (Cys16). Of these, 18 (32%) were also heterozygous for 733C/G (245Val). All of these 18 samples showed weak ‘e’ expression on RBCs when tested with at least one monoclonal antibody to e antigen. cDNA sequencing of three of 18 patient samples showed that the genes encoding Cys16 and Val245 (VS) were on different alleles. We found a high incidence of Cys16 associated with the RHCE ce in our SCD cohort. A high percentage of these patients were also found to be heterozygous for VS. cDNA analysis showed that, in at least three samples, the two mutations were on different alleles, with consequent weakening of expression of the e antigen on RBCs. [ABSTRACT FROM AUTHOR]

Aeromonas hydrophila and A. veronii are widespread and important critical pathogenic bacteria in the aquaculture industry and cause severe economic damage. At present, magnolol has been proved to be a broad‐spectrum antibacterial activity, such as A. hydrophila, Staphylococcus aureus and Streptococcus mutans. In order to explore the cause of in vivo disease resistance of magnolol and promote its safe application in aquaculture, the pathological detection and changes in immune indicators of fish after feeding with magnolol were conducted in this paper. Results showed that the diets supplemented with magnolol (3 g magnolol/kg commercial feed) significantly increase the expression level of anti‐inflammatory cytokines (IL‐10, TGF‐β and IL‐4) in the liver of goldfish (p <.05). Additionally, the expression levels of proinflammatory cytokines (IL‐1β, IL‐8 and IFN‐γ) did not increase significantly. Subsequently, this study investigated the resistance of goldfish to A. hydrophila and A. veronii infection after feeding with magnolol. The results showed that the survival rates of treatment groups fed 3 g magnolol/kg commercial feed daily increased by 23.1% and 38.5% after 10 days post A. hydrophila and A. veronii (p =.0351) infection, respectively. Meanwhile, growth performance (body weight and length), major internal organs (liver, spleen, kidney and intestine) and the serum biochemistry indicators (ATL and AST) all exhibited no significant adverse effects after the goldfish fed with magnolol for 30 days. TP showed an increasing concentration in the treatment group (p <.05). Results of the mRNA expression of stress response indicated that the expression level of cyp1a and hsp70 was significantly down‐regulated after a 30‐day treatment (p <.05), and the two genes recovered to the similar level as the control group after a commercial feed diet. In brief, the diets supplemented with magnolol protected the host from the excessive immune response caused by A. hydrophila and A. veronii via enhancing its anti‐inflammatory capacity and had no adverse effects with feeding. [ABSTRACT FROM AUTHOR]

Background: Lewis serologic reagents frequently give inaccurate phenotyping results. Furthermore these serologic reagents are often used in nonserologic assays such as inhibition and immunohistochemistry. In both scenarios knowledge of the fine specificity and cross-reactivity of these reagents will improve the quality of results obtained.Study Design and Methods: A range of contemporary and historical workshop and developmental Lewis reagents including mouse monoclonal (MoAb) and human and goat polyclonal (PoAb) reagents were evaluated. All were evaluated both against Lewis kodecytes expressing only single Le(a) , Le(b) , ALe(b) , BLe(b) , Le(x) , Le(y) , ALe(y) , or BLe(y) antigens and against the same antigens inkjet printed on a paper-based microplate and analyzed by enzyme immunoassay. Nine clinical samples were also evaluated. A kodecyte antigen dilution sensitivity assay was used to establish the ratio of Le(b) antigen between group A1 /A2 and O RBCs.Results: A continuum of cross-reactivity from Le(x) through to H was observed with MoAbs. All PoAb and few MoAb anti-Le(a) samples and reagents cross-reacted to some degree with Le(b) antigen. Some PoAb and MoAb anti-Le(b) did not cross-react with Le(a) . All polyclonal goat anti-Le(b) reagents showed substantial activity against ALe(b) and BLe(b) , while no MoAb reagent had this activity. A1 RBCs had less than half the Le(b) antigen of A2 /O RBCs.Conclusions: Substantial cross-reactivity of both MoAbs and PoAbs with related antigens highlights the risks of using serologic reagents in nonserologic assays or against synthetic antigens. The lack of ALe(b) activity in anti-Le(b) MoAbs explains their poor performance against blood group A1 Le(a-b+) phenotypes. [ABSTRACT FROM AUTHOR]

Vitiligo is caused by an autoimmune reaction against melanocytes leading to melanocyte loss. The cause of vitiligo is an interaction between genetic susceptibility and environmental factors. Both the adaptive immune system—through cytotoxic CD8+ T cells and melanocyte specific antibodies—and the innate immune system are involved in these immune processes in vitiligo. While recent data stressed the importance of innate immunity in vitiligo, the question remains why vitiligo patients' immune response becomes overly activated. Could a long‐term increase in innate memory function, described as trained immunity after vaccination and in other inflammatory diseases, play a role as an enhancer and continuous trigger in the pathogenesis of vitiligo? After exposure to certain stimuli, innate immune system is able to show an enhanced immunological response to a secondary trigger, indicating a memory function of the innate immune system, a concept termed trained immunity. Trained immunity is regulated by epigenetic reprogramming, including histone chemical modifications and changes in chromatin accessibility that cause sustained changes in the transcription of specific genes. In responses to an infection, trained immunity is beneficial. However, there are indications of a pathogenic role of trained immunity in inflammatory and autoimmune diseases, with monocytes presenting features of a trained phenotype, resulting in increased cytokine production, altered cell metabolism through mTOR signaling, and epigenetic modifications. This hypothesis paper focusses on vitiligo studies that have shown these indications, suggesting the involvement of trained immunity in vitiligo. Future studies focusing on metabolic and epigenetic changes in innate immune cell populations in vitiligo could help in elucidating the potential role of trained immunity in vitiligo pathogenesis. [ABSTRACT FROM AUTHOR]

In binocular stereo matching, there has been a problem of low matching accuracy and noise immunity in discontinuous regions and weak‐textured regions. This paper proposes a stereo matching algorithm based on an improved adaptive support window. In the cost computation stage, first, according to the preset arm length and colour threshold, a cross‐based arm is obtained, which centres on the pixel to be matched; then the adaptive regions of the vertical arm and the horizontal arm are constructed respectively, which have different shape and size. Finally, the union of the two adaptive regions is used as the final support window of Census transform. Performance evaluations on Middlebury stereo data sets demonstrate that the proposed algorithm outperforms other seven most challenging stereo matching algorithms. The mismatching rate of this algorithm is greatly reduced, and the anti‐noise performance is also improved considerably. Because the construction of the adaptive region is based on strict criteria and comprehensive consideration, the algorithm proposed in the paper can improve the matching accuracy in the weak‐textured regions and discontinuous disparity regions. [ABSTRACT FROM AUTHOR]

There is growing scientific interest in immunity mandates/passports (IMP) for viral diseases in light of the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) pandemic. IMP isolate those who remain nonimmune from various settings to reduce nonhousehold transmissions from the nonimmune and reduce severe/critical illness among the nonimmune. A major limitation in the scientific literature is that there are currently no methods to quantify how many nonimmune individuals need to be isolated to achieve these purported benefits. This paper develops a procedure for estimating the benefits of IMP using a novel variant of the number needed to treat which we call the number needed to isolate (NNI). We use data from the SARS‐CoV‐2 pandemic to demonstrate the properties and utility of the NNI and to inform the debate about IMP. We focus on data from the European Union, United Kingdom, United States, Canada, Australia, and Israel during the fall 2021 when the Delta (B.1.617.2) variant predominated. [ABSTRACT FROM AUTHOR]

Background: Currently, patients with diabetic erectile dysfunction (DMED) were not satisfied with the effects of first-line phosphodiesterase type 5 inhibitors (PDE5Is). Hence, this paper was designed to mine hub biomarkers in DMED and explore its potential mechanisms. Methods: Gene expression matrix of DMED was downloaded from the gene expression omnibus (GEO; GSE2457) dataset. The top 20 genes were selected based on the connectivity degrees in protein-protein interaction (PPI) network. Functional enrichment analysis was utilized to reveal DMED-related signaling pathways. We also explored the roles of immunity, m6A, ferroptosis, or cuproptosis in DMED and constructed Sprague Dawley (SD) rats DMED model to verify gene expressions by quantitative real-time polymerase chain reaction (qRT-PCR). Results: Based on the threshold, a total of 122 differently expressed genes (DEGs) were identified in DMED, including 39 up-regulated and 83 down-regulated genes. Functional enrichment analysis implied that these DEGs were significantly enriched in peroxisome proliferator-activated receptors, ferroptosis, hypoxia-inducible factor 1 signaling pathways, and so on. SD rats DMED model was also successfully established by us and validated by intracavernous pressure/mean arterial pressure, Masson's trichrome staining, and immunohistochemical analysis. We further verified the expression of these top 20 genes from the PPI network by qRT-PCR in the SD rats DMED model and finally identified Sparc, Lox, Srebf1, and Mmp3 as hub biomarkers (all p<0.05). As for immunity and cuproptosis, our analysis indicated thatDMEDhad nothing to do with them (all p > 0.05). Actually, DMED was markedly associated with m6A regulators and ferroptosis. Conclusions:We identified Sparc, Lox, Srebf1, and Mmp3 as potential hub biomarkers in the SD rats DMED model for future drug development and found its significant associations with m6A regulators and ferroptosis, but not with immunity or cuproptosis. [ABSTRACT FROM AUTHOR]

Considering the effect of stochasticity including white noise and colored noise, this paper aims to study a hybrid stochastic cholera epidemic model with waning vaccine‐induced immunity and nonlinear telegraph perturbations. First, we derive a critical value ℛ0C related to the basic reproduction number ℛ0 of the deterministic model. The key aim of this paper is to generalize the θ‐stochastic criterion method proposed by the recent work (Han et al. in Chaos Solit Fract 140:110238, 2020) to eliminate nonlinear telegraph perturbations. Next, via constructing several θ‐stochastic Lyapunov functions and using the generalized method, we further prove that the stochastic model have a unique ergodic stationary distribution under ℛ0C>1. Results show that the prevention and control of cholera epidemic depend on low transmission rate and small telegraph perturbations. Finally, the corresponding numerical simulations are performed to illustrate our analytical results and a practical application on the Somalia cholera outbreak is shown at the end of this paper. [ABSTRACT FROM AUTHOR]

Introduction: Already in its first implementation, the introduction of the Covid‐19 immunity certificate has generated some debate among the public. This debate might be a hindrance to the effective realization of this policy. This study aimed to systematically review published research evaluating public feeling of the Covid‐19 immunity certificate policy measure and to find which factors might influence its acceptance. Methods: We followed the scoping review methods manual by the Joanna Briggs Institute. We included studies with no time limits that presented novel data, and no exclusions have been made based on study design. We excluded articles that presented just expert opinions. Results: We found and reviewed 17 articles. The included studies were conducted in two main countries (the United Kingdom and Switzerland), with the rest from Israel, Italy, Spain, Germany, Australia, Taiwan and China. Both qualitative and quantitative studies were included, and nonrepresentative samples were mostly used to explore the public feeling about the Covid‐19 immunity certification. The included studies showed that public views on immunity certification are quite contradictory and influenced by age, gender, ethnicity, political orientation and attitudes towards Covid‐19 vaccination. The topic more often addressed by the included studies was the public's views on the positive and negative implications of the Covid‐19 immunity certificate in terms of ethical, legal and behavioural consequences of this measure. Conclusion: The varying acceptance rates are notable and may partly be linked to differences in demographics, Covid‐19 concerns and ideological beliefs, as seen in other health‐related tracking policies. Moreover, dominant factors behind the (un)success of this policy are complex and entangled with the cultural and political dimensions rather than being just technical. For this reason, it is important to expand psychosocial research to better understand the concerns behind health certifications and allow planning of culturally based and ethically sound suitable strategies. This would be very relevant to increasing public approval and compliance with this public health measure. Patient or Public Contribution: This does not apply to our work as it was a review paper. [ABSTRACT FROM AUTHOR]

In this paper, we formulate a generalized hepatitis B virus (HBV) infection model with two modes of infection transmission and adaptive immunity and investigate its dynamical properties. Both the virus‐to‐cell and cell‐to‐cell infection transmissions are modeled by general functions which satisfy some biologically motivated assumptions. Furthermore, the model incorporates three distributed time delays for the production of active infected hepatocytes, mature capsids, and virions. The well‐posedness of the proposed model is established by showing the non‐negativity and boundedness of solutions. Five equilibria of the model are identified in terms of five threshold parameters R0,R1,R2,R3$$ {R}_0,{R}_1,{R}_2,{R}_3 $$, and R4$$ {R}_4 $$. Further, the global stability analysis of each equilibrium under certain conditions is carried out by employing suitable Lyapunov function and LaSalle's invariance principle. Finally, we present an example with numerical simulations to illustrate the applicability of our study. Nonetheless, the results obtained in this study are valid for a wide class of HBV infection models. [ABSTRACT FROM AUTHOR]

The fast and intermittent power changes in a direct‐current fast charging (DCFC) station impose adverse dynamic impacts on the station's host grid, particularly a weak AC distribution grid. This paper (i) investigates the impacts of the electric vehicle (EV) conventional DCFC station on its host distribution power system, and (ii) shows that the station can be enhanced by a battery energy storage system and an appropriate control strategy to mitigate the mutual dynamic interactions between the station and its host grid. The enhanced DCFC station is based on a variable‐voltage, common DC‐bus architecture which masks the station's internal dynamics, including rapid and intermittent EV charging processes, from the grid. Thus, it can be interfaced to a host grid, regardless of short‐circuit level, X/R ratio, and power capacity. The focus is also on the dynamic immunity of the DCFC facility to potential disturbances in its host weak‐grid. The reported studies are based on detailed time‐domain simulation of two DCFC stations in the PLECS software platform. [ABSTRACT FROM AUTHOR]

Lists forthcoming research papers on immunology published in the journal "Immunology."

Presents several developments in the veterinary medicine. Identification of keel and furculum damage in laying hens; Detection of antigens in fresh and autolysed tissue; Hypervaccination with marker vaccines against bovine herpesvirus type 1.

If there was any doubt of the primary role that plant secondary metabolites play in host–parasite co‐evolution, the "From the Cover" paper by Tan et al. (2019) featured in this issue of Molecular Ecology will lay these doubts to rest. The group's previous work on monarch butterflies (Danaus plexippus) infected with the protozoan pathogen Ophryocystis elektroscirrha (OE) demonstrated higher survival and lower spore load on high cardenolide‐producing milkweed (Asclepias curassavica) (Figure 1a) compared with low cardenolide‐producing milkweed (A. incarnata) (de Roode, Pedersen, Hunter, & Altizer, 2008) (Figure 1b). The mechanism of this protective effect is not directly clear, but a leading hypothesis is that the cardenolides confer protection through toxicity to the parasite. However, the role of the caterpillar immune system in managing this parasite is largely unknown. Novel insights into the influence of toxic plant metabolites on caterpillar immunity are explored in Tan et al. (2019). Using transcriptomics to probe this model system, the authors found that herbivore immune genes were down‐regulated and detoxification genes were up‐regulated when larvae were reared on the milkweed species with high cardenolide concentrations (A. curassavica). Surprisingly, immune genes were not significantly up‐ or down‐regulated in response to protozoan infection alone. This tantalizing result suggests that sequestered plant metabolites, not immunity, is reining in protozoan infections in these larvae, and promoting survival. As the authors point out, the strategy to invest in sequestration may come at a cost, which is to the detriment of the immune response (Smilanich, Dyer, Chambers, & Bowers, 2009). However, the cost becomes worth the investment when chemical sequestration takes on an antipathogen role. The novelty of the Tan et al. (2019) paper is that they show the investment in sequestration leading to a possible divestment in immunity. [ABSTRACT FROM AUTHOR]

Aim: The objective of this review is to describe the immunological mechanisms which facilitate maternal tolerance at the maternal‐placental interface, and to discuss how these mechanisms are disrupted in pre‐eclampsia. Methods: A literature review was performed based on the analysis of papers available on PubMed. The most important and relevant studies regarding the immunological mechanisms which facilitate maternal tolerance in healthy pregnancy and pre‐eclampsia are presented in this article. Results: The maternal‐placental interface is the site where the immune tolerance begins and develops. Within the innate immunity, natural killer cells, macrophages and dendritic cells play a pivotal role in tolerance through regulation of inflammation. On the other hand, within the adaptive immunity, the correct increase of regulatory T cells is crucial for ensuring immune tolerance toward placental cells. Disturbances in maternal tolerance can lead to the appearance of pregnancy complications such as pre‐eclampsia, which has a considerable impact on perinatal morbidity and mortality. Conclusion: Our partial knowledge of immunological mechanisms involved in tolerance at the maternal‐placental interface indicates that pre‐eclampsia is characterized by alterations of this maternal immune tolerance, which could represent the origin of the disease. [ABSTRACT FROM AUTHOR]

Impaired regulation of immune function characterised by chronic inflammation together with a declining protective immune response is a major challenge to healthy ageing. It is therefore important to understand the mechanisms that regulate immune function and the impact of ageing upon such processes. Appropriate induction and resolution of the immune response require adequate availability of polyunsaturated fatty acids (PUFAs) for incorporation into cell membranes. However, humans are unable to synthesise PUFAs de novo and are dependent upon dietary intake for pre‐formed PUFAs or synthesis by the liver from the essential fatty acids, linoleic acid (LA, 18:2n‐6) and alpha‐linolenic acid (aLNA, 18:3n‐3). We have shown that activation of peripheral blood mononuclear cells increases PUFA biosynthesis from essential fatty acids via a mechanism that involves altered epigenetic regulation of a key gene in the pathway. Moreover, induction of PUFA synthesis is directly involved in the regulation of lymphocyte activation and proliferation. The aim of the Biotechnology and Biological Sciences Research Council responsive mode award described in this paper, 'How does polyunsaturated fatty acid biosynthesis regulate T‐lymphocyte function?', is to determine how PUFA biosynthesis regulates T‐cell function and the effect of ageing on this process. The project will identify points of regulation in the biosynthetic pathway and how these might influence the capacity for up‐regulation of PUFA synthesis in older individuals. We will use stable isotope tracers of LA and aLNA to determine whether newly synthesised PUFAs are preferential substrates for synthesis of lipid mediators and whether they are involved in formation of membrane microdomains that mediate cell signalling. [ABSTRACT FROM AUTHOR]

Immunoglobulin (Ig) is the one of the main anti‐infective components of blood, colostrum and breast milk. It is the unique glycoprotein that defends the body from harmful bacteria, viruses and other environmental pathogens by either binding to them or by forming an encapsulating barrier. The expansion of antimicrobial and immunomodulatory products from natural sources for dietary supplementation in both animals and humans is an ever growing and thriving area of research. Purified Ig from sheep serum (ovine serum Ig) is one such candidate product. Recent work has shown the various biological effects of oral Ig in different animal models including its effect on growth, immunity, intestinal growth and gut barrier function. The objective of this paper is to review the results of recent studies demonstrating the effects of oral Ig in both pathogenic and non‐pathogenic animal models and to suggest a possible mechanism of its action. Overall, purified oral Ig improves growth of healthy (and challenged) rats and defends against enteric infection by immunomodulation, mucin protein and/or modification of commensal microbial composition. The findings contribute to knowledge of how orally administered ovine Ig can influence and enhance key indicators of gut function and overall growth performance in an animal model. [ABSTRACT FROM AUTHOR]

The prostate gland is a strictly androgen-dependent organ which is also the main target of infectious and inflammatory diseases in the male reproductive tract. Host defenses and immunity of the gland have unique features to maintain a constant balance between response and tolerance to diverse antigens. In this context, the effects of reproductive hormones on the male tract are thus complex and have just started to be defined. From the classical description of 'the prostatic antibacterial factor,' many host defense proteins with potent microbicidal and anti-tumoral activities have been described in the organ. Indeed, it has been proposed a central role for resident cells, that is, epithelial and smooth muscle cells, in the prostatic response against injuries. However, these cells also represent the target of the inflammatory damage, leading to the development of a Proliferative Inflammatory Atrophy-like process in the epithelium and a myofibroblastic-like reactive stroma. Available data on androgen regulation of inflammation led to a model of the complex control, in which the final effect will depend on the tissue microenvironment, the cause of inflammation, and the levels of androgens among other factors. In this paper, we review the current scientific literature about the inflammatory process in the gland, the modulation of host defense proteins, and the influence of testosterone on the resolution of prostatitis. [ABSTRACT FROM AUTHOR]

Our understanding of immunity to filarial infection is enigmatic and continues to be passionately debated. The mechanisms whereby filarial nematodes are killed in vivo and how these parasites avoid these mechanisms are poorly understood. Although vaccination studies in permissive animals took off seven decades ago, the exact mechanisms driving protective immunity are extensively being investigated. Currently, little is known regarding the collective functions or counter-regulatory mechanisms of the antibody isotypes in filarial infection with respect to protective immunity. Establishing the functional role of antibody isotypes and cytokines in the various infection phenotypes can contribute immensely to current knowledge in filarial immunology. This paper reviews insight into protective immunity in filarial infection with focus on humoral and cellular responses from animal models and human studies. [ABSTRACT FROM AUTHOR]

1. Immune priming refers to improved protection of the host after a second encounter with the same parasite or pathogen. This phenomenon is similar to that of adaptive immunity in vertebrates. 2. There is evidence to suggest that this improved protection can be species/strain-specific and can protect organisms for a lifetime. These two attributes, along with a biphasic immune response, are essential characteristics of immune priming and form the basis for the effectiveness of resistance to parasites and pathogens. 3. This paper considers the effect of immune priming within and across generations, the influence of a heterologous challenge during immune priming and the importance of testing the immune response with natural pathogens. 4. The analysis presented takes into account the multifaceted nature of the invertebrate immune response. The lack of evidence suggesting that the bacterial microbiome plays a complementary role in the immune priming outcome is discussed. 5. Finally, the cost of immune priming is explored. This is a poorly investigated issue, which could help to explain why there is a paucity of evidence in support of immune priming. [ABSTRACT FROM AUTHOR]

The digestive tract works through a complex network of integrative functions. At the level of the gut, this integration occurs between the immune, neuromotor and enteroendocrine systems, coordinating the physical and chemical elements of the intestinal barrier in order to facilitate digestion whilst protecting the gut from unwanted components of the luminal contents. Gastrointestinal function is controlled and coordinated by the central nervous system to ensure effective motility, secretion, absorption and mucosal immunity. It follows that perturbations in this complex network could lead to gut dysfunction and symptom generation. Recently, attention has been focused on the emerging hypothesis that gut luminal content contributes to determine normal GI function and on the therapeutic possibilities arising from modulating its impact on gut physiology and immunity using probiotic bacteria. In this issue of Neurogastroenterology and Motility, two papers explore the effect of specific probiotic bacteria on spinal neuronal activation and in vitro muscle contractility. These papers support the notion that the composition of the intestinal microbiota can influence gut neuro-motor function and enhance our understanding on the mechanisms of action underlying the effects of specific probiotics on gut functional disorders. [ABSTRACT FROM AUTHOR]

The Steering Committee for the Prevention and Control of Infectious Diseases in Asia recently conducted a survey of primary-care physicians in Asia, which revealed that many physicians administer boosters in their clinical practice and that there is considerable variation and uncertainty among physicians regarding this practice. This paper serves as a response to physicians’ uncertainties by reviewing the literature regarding the administration of hepatitis B vaccine boosters in high endemicity areas and presenting the Steering Committee's guidelines for booster administration. While there are few data to support a need for routine hepatitis B vaccine boosters as a public health measure, they help to provide reassurance of immunity against breakthrough infection in certain risk groups. In clinical practice, primary-care physicians must exercise their judgment regarding the need for booster vaccination on an individual basis. This paper examines the available literature on the administration and value of hepatitis B vaccine boosters, explores the differences between the public health approach and clinical practice, and provides guidelines for those who use boosters in high endemicity Asian populations. Relevant articles were identified through searches of MEDLINE (1975–2003) and the Cochrane Library, using‘hepatitis B’ and‘booster’ as primary search terms. Guidelines for those who decide to administer hepatitis B vaccine boosters include: boosting approximately 10–15 years after primary vaccination; boosting rather than not when monitoring of antibody levels is not feasible; boosting immunocompromised patients when the antibody to hepatitis B surface antigen titer falls below 10 mIU/mL; and boosting healthcare workers based on the endemicity of the particular country. [ABSTRACT FROM AUTHOR]

Summary: This paper discusses the following ten subtitles with the contents indicated. 1. To meet a microbe: discusses the four alternatives in host-microbe interactions. 2. Receptors and signal transduction giving gene activation: discusses the lipopolysaccharide receptor and the limitations of cell cultures versus use of live animals. 3. Effector molecules -- antimicrobial peptides with and without cysteines. A data base exists with over 500 sequences. This paper gives a general overview of five classes of gene-encoded effector molecules, based on the absence or presence of cysteines. These molecules are peptide antibiotics with wide spectra against different microbes. They are synthesized as propeptides and post-translational modifications are common. 4. Effectors of innate immunity -- lethal action without host damage: evaluates current opinions about the mode of action of peptide antibiotics and the fact that these effectors do not create host damage. 5. Genes, introns and movable elements. Two cecropin genes containing movable elements and the human cathelicidin gene for proFALL-39/hCAP18 are discussed. 6. The natural microflora. Hippos or frogs as model systems. This section includes the isolation of bacteria from the normal flora of frogs; Aeromonas hydrophila, the bacterium found on all five frog species studied; arguments and selected examples of frog-microbe interactions in vivo and in vitro; and the use of glucocorticoids as control for nuclear factor-κB/IκBα regulation of effector genes. 7. The use of germ-free mice -- hard facts from hard work: summarizes new findings which indicate that germ-free mice are born with a seat of antibacterial peptides in their small intestine. The intestine of germ-free mice monoinfected with A. hydrophila have peptide patterns that differ depending on a pretreatment with cortisone. 8. Looking... [ABSTRACT FROM AUTHOR]

This article presents an index of authors who have contributed to the publication of the "Journal of Fish Diseases." C. Agius, M.T. Horne and P.D. Ward contributed to the research paper "Immunization of Rainbow Trout, Salmo gairdneri Richardson, Against Vibriosis: Comparison of an Extract Antigen With Whole Cell Bacterins by Oral and Intraperitoneal Routes." D.F. Amend, K.A. Johnson, T.R. Croy and D.H. McCarthy presented the research paper "Some Factors Affecting the Potency of Yersinia ruckeri Bacterins."

`The O9-specific mannan of Escherichia coil was synthesized in vitro from GDP-[14C]mannose by membranes which were obtained from a phosphomannose isomerase-less mutant of E. coli O9:K29- :H-, Subsequent treatment of the membranes with dilute acid liberated a neutral product, whereas with aqueous phenol a charged product was obtained. Chromatography on DEAE-cellulose, incubation with alkaline phosphatase and microdetermination showed that the charged mannan was substituted with one phosphate per chain. The neutral 14C-labelled product of the incubation hr vitro was reduced with sodium boro[³H]hydride. After total acid hydrolysis, the radioactive material was chromatographed on paper in the presence of borate. It was found that [³H]glucitol, but no [³H, 14C]mannitol was present. When the neutral product, which was obtained after incubation of 14C-prelabelled membranes with nonradioactive GDP-mannose, was hydrolyzed with and without prior reduction with non-radioactive sodium borohydride, in subsequent paper chromatography, [14C]glucitol or [14C]glucose was found. The glucose was also converted enzymatically to gluconic acid, which was identified by paper electrophoresis. These results show that in the neutral O9-specific mannan glucose is at the reducing end and they indicate that the mannan chain grows at the non-reducing end. This is discussed with respect to the overall mechanism of the biosynthesis of the 09 antigen. [ABSTRACT FROM AUTHOR]

• In this paper we describe PATTERN-TRIGGERED IMMUNITY (PTI) COMPROMISED RECEPTOR-LIKE CYTOPLASMIC KINASE 1 (PCRK1) of Arabidopsis thaliana, an RLCK that is important for defense against the pathogen Pseudomonas syringae pv. maculicola ES4326 (Pma ES4326). • We examined defense responses such as bacterial growth, production of reactive oxygen species (ROS) and callose deposition in pcrk1 mutant plants to determine the role of PCRK1 during pathogen infection. • Expression of PCRK1 was induced following pathogen infection. Pathogen growth was significantly higher in pcrk1 mutant lines than in wild-type Col-0. Mutant pcrk1 plants showed reduced pattern-triggered immunity (PTI) against Pma ES4326 after pretreatment with peptides derived from flagellin (flg22), elongation factor-Tu (elf18), or an endogenous protein (pep1). Deposition of callose was reduced in pcrk1 plants, indicating a role of PCRK1 in activation of early immune responses. A PCRK1 transgene containing a mutation in a conserved lysine residue important for phosphorylation activity of kinases (K118E) failed to complement a pcrk1 mutant for the Pma ES4326 growth phenotype. • Our study shows that PCRK1 plays an important role during PTI and that a conserved lysine residue in the putative kinase domain is important for PCRK1 function. [ABSTRACT FROM AUTHOR]

The type VI secretion system (T6SS) has recently been demonstrated to mediate interbacterial competition and to discriminate between self and nonself. T6SS+ bacteria employ toxic effectors to inhibit rival cells and concurrently use effector cognate immunity proteins to protect their sibling cells. The effector and immunity pairs (E-I pairs) endow the bacteria with a great advantage in niche competition. Tle4-Tli4 (PA1510-PA1509) is a newly identified E-I pair that is controlled by H2-T6SS in Pseudomonas aeruginosa. Tle4 exhibits phospholipase activity, which destroys the cell membrane of rival cells, and the periplasm-located Tli4 in donor cells eliminates this toxic effect of Tle4. In this paper, the structure of the Tle4-Tli4 complex is reported at 1.75 Å resolution. Tle4 consists of two domains: a conserved α/β-hydrolase domain and an unusual cap domain in which two lid regions (lid1 and lid2) display a closed conformation that buries the catalytic triad in a deep funnel. Tli4 also displays a two-domain structure, in which a large lobe and a small lobe form a crab claw-like conformation. Tli4 uses this crab claw to grasp the cap domain of Tle4, especially the lid2 region, which prevents the interfacial activation of Tle4 and thus causes enzymatic dysfunction of Tle4 in sister cells. [ABSTRACT FROM AUTHOR]

Host immunity is a major driver of pathogen evolution and thus a major determinant of pathogen diversity. Explanations for pathogen diversity traditionally assume simple interactions between pathogens and the immune system, a view encapsulated by the susceptible-infected-recovered (SIR) model. However, there is growing evidence that the complexity of many host-pathogen interactions is dynamically important. This revised perspective requires broadening the definition of a pathogen's immunological phenotype, or what can be thought of as its immunological niche. After reviewing evidence that interactions between pathogens and host immunity drive much of pathogen evolution, I introduce the concept of a pathogen's immunological phenotype. Models that depart from the SIR paradigm demonstrate the utility of this perspective and show that it is particularly useful in understanding vaccine-induced evolution. This paper highlights questions in immunology, evolution, and ecology that must be answered to advance theories of pathogen diversity. [ABSTRACT FROM AUTHOR]

Background The role of T helper (Th) 17 cells in autoimmune diseases has been extensively studied recently, but its function in oestrogen-deficient osteoporosis remains undefined. This review aimed to explore the role of Th17 cells in regulating bone loss induced by oestrogen deficiency. Materials and methods We searched PubMed, Embase, Google Scholar and Biosis up to 1 February 2013 for immune regulation of oestrogen-deficient osteoporosis by Th17 cells. Terms relevant to immunity, oestrogen deficiency, osteoporosis and Th17 cells were used for database searching. Seventy-five papers met the predetermined searching criteria. Results Studies indicate Th17 lineage to be a potent osteoclastogenic mediator in oestrogen-deficient osteoporosis. Oestrogen deficiency promotes osteoclastogenesis by up-regulating Th17 cell populations in bone marrow and IL-17 levels in peripheral blood. Meanwhile, transcription factors involved in Th17 cell differentiation, such as RORγt and RORα, are highly expressed in ovariectomized animals. Treatment with IL-17 significantly promotes production of RANKL, TNF and IL-6 as well as TRAP+ cells in culture; blocking IL-17 pathway significantly reduces abundance of Th17 cells and effectively prevents bone loss in ovariectomized mice. Conclusions The main body of literatures suggests Th17 to be a critical modulator in the pathogenesis of oestrogen-deficient osteoporosis, which supports the notion that oestrogen-deficient osteoporosis is a complex interplay between oestrogen, osteoclastogenic cytokines and osteoclasts. In addition, therapeutic strategies targeting IL-17 networks may be clinically useful in treatment for postmenopausal osteoporosis. [ABSTRACT FROM AUTHOR]

Please cite this paper as: Sarah C. Gilbert. (2012) Advances in the development of universal influenza vaccines. Influenza and Other Respiratory Viruses DOI:10.1111/irv.12013. Despite the widespread availability and use of influenza vaccines, influenza still poses a considerable threat to public health. Vaccines against seasonal influenza do not offer protection against pandemic viruses, and vaccine efficacy against seasonal viruses is reduced in seasons when the vaccine composition is not a good match for the predominant circulating viruses. Vaccine efficacy is also reduced in older adults, who are one of the main target groups for vaccination. The continual threat of pandemic influenza, with the known potential for rapid spread around the world and high mortality rates, has prompted researchers to develop a number of novel approaches to providing immunity to this virus, focusing on target antigens which are highly conserved between different influenza A virus subtypes. Several of these have now been taken into clinical development, and this review discusses the progress that has been made, as well as considering the requirements for licensing these new vaccines and how they might be used in the future. [ABSTRACT FROM AUTHOR]

LINKED CONTENT This article is linked to Wunschi et al and Tornai & Papp papers. To view these articles, visit https://doi.org/10.1111/apt.16153 and https://doi.org/10.1111/apt.16201 [ABSTRACT FROM AUTHOR]

LINKED CONTENT This article is linked to Wunschi et al and Wunsch & Milkiewicz papers. To view these articles, visit https://doi.org/10.1111/apt.16153 and https://doi.org/10.1111/apt.16211 [ABSTRACT FROM AUTHOR]

Please cite this paper as: Zambon. (2012) Surveillance for antiviral resistance. Influenza and Other Respiratory Viruses 7(Suppl. 1), 37-43. In the 10 years since licensure of neuraminidase inhibitor drugs, their use has steadily increased, especially during the pandemic of 2009. Experience now indicates that factors which influence the emergence of high level resistance include the nature of drug binding to target, viral subtype, the use of post exposure prophylaxis and a lack of immunity in the host as seen in children and immunocompromised individuals. These factors point towards targetted surveillance programmes for the early identification of transmissible drug resistance. [ABSTRACT FROM AUTHOR]

Polysaccharides (PS) have historically been viewed as T cell-independent antigens. However, in this paper I propose a new concept, based on substantial data from my laboratory over the previous 10 years, that during infections with PS-encapsulated extracellular bacteria, PS-specific IgG responses are largely CD4+ T cell dependent. Thus, capsular PS is typically encountered by the immune system covalently attached to the underlying subcapsular bacterial domain. I speculate that noncovalent association of PS with immunogenic proteins within the bacterial particle leads to recruitment of protein-specific CD4+ T cell help for the anti-PS response. However, differences in the composition and/or structure of the subcapsular domain of different extracellular bacteria may result in distinct anti-PS responses as well as differential effects on the immune response to coimmunizing soluble antigens. CD4+ T cell help for IgG anti-PS responses during infections with extracellular bacteria is likely to promote opsonic clearance of these rapidly growing pathogens. However, the expression of immunosuppressive components by certain bacteria may also serve to dampen such responses. [ABSTRACT FROM AUTHOR]

Sonesson M, Ericson D, Kinnby B, Wickström C. Glycoprotein 340 and sialic acid in minor-gland and whole saliva of children, adolescents, and adults. Eur J Oral Sci 2011; 119: 435-440. © 2011 Eur J Oral Sci Glycoprotein 340 (gp-340) is a bacterial-binding glycoprotein found in major-gland and minor-gland saliva. Sialic acid, a common terminal structure of salivary glycoproteins, interacts with microorganisms and host ligands, as well as with free radicals. This study investigated the contents of gp-340 and sialic acid in minor-gland saliva and whole saliva of children (3 yr of age), adolescents (14 yr of age), and adults (20-25 yr of age). Labial-gland saliva and buccal-gland saliva were collected on filter paper, and unstimulated whole saliva was collected by draining into a tube. The relative amount of gp-340 and sialic acid was determined by ELISA and by enzyme-linked lectin assay (ELLA), respectively. In minor-gland saliva, no statistically significant differences in gp-340 and sialic acid were seen between the age-groups. Among adults, significantly lower amounts of gp-340 and sialic acid were seen in labial saliva compared with buccal saliva. In whole saliva, the amount of gp-340 was significantly lower among adults compared with children. No differences between genders were seen. Stable content of gp-340 and sialic acid in minor-gland saliva across the age-groups, and a higher content of gp-340 in the whole saliva of the youngest age-group (3-yr-olds) compared with the adult group, may reflect that those components are vital innate factors of immunity in children's saliva. [ABSTRACT FROM AUTHOR]

Please cite this paper as: Shields (2011). Lymphatics: At the Interface of Immunity, Tolerance, and Tumor Metastasis. Microcirculation 18( 7), 517-531. Abstract The lymphatic system has long been accepted as a passive escape route for metastasizing tumor cells. The classic view that lymphatics solely regulate fluid balance, lipid metabolism, and immune cell trafficking to the LN is now being challenged. Research in the field is entering a new phase with increasing evidence suggesting that lymphatics play an active role modulating inflammation, autoimmune disease, and the anti-tumor immune response. Evidence exists to suggest that the lymphatics and chemokines guide LN bi-functionally, driving immunity vs. tolerance according to demand. At sites of chronic inflammation, autoimmunity, and tumors, however, the same chemokines and aberrant lymphangiogenesis foster disease progression. These caveats point to the existence of a complex, finely balanced relationship between lymphatics and the immune system in health and disease. This review discusses emerging concepts in the fields of immunology, tumor biology, and lymphatic physiology, identifying critical, overlapping functions of lymphatics, the LN and lymphoid factors in tipping the balance of immunity vs. tolerance in favor of a growing tumor. [ABSTRACT FROM AUTHOR]

Major challenges in periodontology include understanding the pathophysiology, the interplay between various components of the host response, parallels with other diseases and identifying biomarkers of the disease. Four reviews were compiled with the aim of better understanding: (1) the role of polymorphic nuclear leucocytes (PMNs), i.e. neutrophils; (2) the function of cytokine networks in the host response; (3) whether parallels exist with rheumatoid arthritis (RA); and (4) whether useful biomarkers currently exist to help in the management of periodontal disease. Based on the focused questions, electronic and manual searches were conducted for human, animal and cellular studies on the above topics. Papers fulfilling the inclusion criteria were selected and reviews were written and reviewed and corrected before the academy meeting to produce consensus statements. The following consensus statements were produced. PMNs are important in the pathophysiology of periodontal disease but there is limited evidence on their much quoted destructive potential. Cytokine networks are enormously complex and we are really at the beginning of understanding their role in the disease process. RA has both similarities and marked differences to periodontal disease although the existing utilization of anti-cytokine therapies and other molecules in its treatment may have importance in periodontal disease therapy. Biomarkers for periodontal disease have yet to be completely defined but the ratio of receptor activator of NF- κB ligand to osteoprotegerin appears to be a biomarker test with utility for detecting bone destruction. [ABSTRACT FROM AUTHOR]

Please cite this paper as: De Vleeschauwer et al. (2011) Cross-protection between antigenically distinct H1N1 swine influenza viruses from Europe and North America. Influenza and Other Respiratory Viruses 5(2), 115-122. An avian-like H1N1 swine influenza virus (SIV) is enzootic in swine populations of Western Europe. The virus is antigenically distinct from H1N1 SIVs in North America that have a classical swine virus-lineage H1 hemagglutinin, as does the pandemic (H1N1) 2009 virus. However, the significance of this antigenic difference for cross-protection among pigs remains unknown. We examined protection against infection with a North American triple reassortant H1N1 SIV [A/swine/Iowa/H04YS2/04 (sw/IA/04)] in pigs infected with a European avian-like SIV [A/swine/Belgium/1/98 (sw/B/98)] 4 weeks earlier. We also examined the genetic relationships and serologic cross-reactivity between both SIVs and with a pandemic (H1N1) 2009 virus [A/California/04/09 (Calif/09)]. After intranasal inoculation with sw/IA/04, all previously uninfected control pigs showed nasal virus excretion, high virus titers in the entire respiratory tract at 4 days post-challenge (DPCh) and macroscopic lung lesions. Most pigs previously infected with sw/B/98 tested negative for sw/IA/04 in nasal swabs and respiratory tissues, and none had lung lesions. At challenge, these pigs had low levels of cross-reactive virus neutralizing and neuraminidase inhibiting (NI) antibodies to sw/IA/04, but no hemagglutination-inhibiting antibodies. They showed similar antibody profiles when tested against Calif/09, but NI antibody titers were higher against Calif/09 than sw/IA/04, reflecting the higher genetic homology of the sw/B/98 neuraminidase with Calif/09. Our data indicate that immunity induced by infection with European avian-like H1N1 SIV affords protection for pigs against North American H1N1 SIVs with a classical H1, and they suggest cross-protection against the pandemic (H1N1) 2009 virus. [ABSTRACT FROM AUTHOR]

Please cite this paper as: Pearce et al. (2011) Understanding mortality in the 1918-1919 influenza pandemic in England and Wales. Influenza and Other Respiratory Viruses 5(2), 89-98. The causes of recurrent waves in the 1918-1919 influenza pandemic are not fully understood. To identify the risk factors for influenza onset, spread and mortality in waves 1, 2 and 3 (summer, autumn and winter) in England and Wales in 1918-1919. Influenza mortality rates for 333 population units and putative risk factors were analysed by correlation and by regressions weighted by population size and adjusted for spatial trends. For waves 1 and 3, influenza mortality was higher in younger, northerly and socially disadvantaged populations experiencing higher all-cause mortality in 1911-1914. Influenza mortality was greatest in wave 2, but less dependent on underlying population characteristics. Wave duration was shorter in areas with higher influenza mortality, typically associated with increasing population density. Regression analyses confirmed the importance of geographical factors and pre-pandemic mortality for all three waves. Age effects were complex, with the suggestion that younger populations with greater mortality in wave 1 had lesser mortality in wave 2. Our findings suggest that socially disadvantaged populations were more vulnerable, that older populations were partially protected by prior immunity in wave 1 and that exposure of (younger) populations in one wave could protect against mortality in the subsequent wave. An increase in viral virulence could explain the greater mortality in wave 2. Further modelling of causal processes will help to explain, in considerable detail, how social and geographical factors, season, pre-existing and acquired immunity and virulence affected viral transmission and pandemic mortality in 1918-1919. [ABSTRACT FROM AUTHOR]

Please cite this paper as: Is there a ‘gut–brain–skin axis’? Experimental Dermatology 2010; 19: 401–405. Emerging evidence arising from interdisciplinary research supports the occurrence of communication axes between organs, such as the brain–gut or brain–skin axis. The latter is employed in response to stress challenge, along which neurogenic skin inflammation and hair growth inhibition is mediated. We now show that ingestion of a Lactobacillus strain in mice dampens stress-induced neurogenic skin inflammation and the hair growth inhibition. In conclusion, we are introducing a hypothesis, encouraged by our pilot observations and resting upon published prior evidence from the literature, which amalgamates previously proposed partial concepts into a new, unifying model, i.e. the gut–brain–skin axis. This concept suggests that modulation of the microbiome by deployment of probiotics can not only greatly reduce stress-induced neurogenic skin inflammation but even affect a very complex cutaneous phenomenon of (mini-) organ transformation, i.e. hair follicle cycling. These observations raise the intriguing prospect that feeding of just the right kind of bacteria can exert profound beneficial effects on skin homoeostasis, skin inflammation, hair growth and peripheral tissue responses to perceived stress. [ABSTRACT FROM AUTHOR]

Please cite this paper as: Kash et al. (2010) Prior infection with classical swine H1N1 influenza viruses is associated with protective immunity to the 2009 pandemic H1N1 virus. Influenza and Other Respiratory Viruses 4(3), 121–127. Background The 2009 H1N1 pandemic emerged even though seasonal H1N1 viruses have circulated for decades. Epidemio-logical evidence suggested that the current seasonal vaccine did not offer significant protection from the novel pandemic, and that people over the age of 50 might were less susceptible to infection. Objectives In a mouse challenge study with the 2009 pandemic H1N1 virus, we evaluated protective immune responses elicited by prior infection with human and swine influenza A viruses. Results Mice infected with A/Mexico/4108/2009 (Mex09) showed significant weight loss and 40% mortality. Prior infection with a 1976 classical swine H1N1 virus resulted in complete protection from Mex09 challenge. Prior infection with either a 2009 or a 1940 seasonal H1N1 influenza virus provided partial protection and a >100-fold reduction in viral lung titers at day 4 post-infection. Conclusions These findings indicate that in experimental animals recently induced immunity to 1918-derived H1N1 seasonal influenza viruses, and to a 1976 swine influenza virus, afford a degree of protection against the 2009 pandemic virus. Implications of these findings are discussed in the context of accumulating data suggesting partial protection of older persons during the 2009 pandemic. [ABSTRACT FROM AUTHOR]

The ability of B cells to negatively regulate cellular immune responses and inflammation has only recently been described. Hallmark papers from a number of distinguished laboratories have identified phenotypically diverse B-cell subsets with regulatory functions during distinct autoimmune diseases, including IL-10-producing B cells, CD5+ B-1a cells, CD1d+ marginal zone B cells, and transitional-2-marginal zone precursor B cells. Most recently, a numerically rare and phenotypically unique CD1dhiCD5+CD19hi subset of regulatory B cells has been identified in the spleens of both normal and autoimmune mice. CD1dhiCD5+ B cells with the capacity to produce IL-10 have been named B10 cells as they produce IL-10 exclusively and are the predominant B-cell source of IL-10. Remarkably, B10 cells are potent negative regulators of inflammation and autoimmunity in mouse models of disease in vivo. Herein, our current understanding of B10-cell development and function is reviewed in the context of previous studies that have identified and characterized regulatory B cells, emerging evidence for B10-cell regulation of tumor immunity, and the likelihood that B10 cells exist in humans. [ABSTRACT FROM AUTHOR]

Neuroimmunomodulation describes the field focused on understanding the mechanisms by which the central nervous system interacts with the immune system, potentially leading to changes in animal behavior. Nonetheless, not many articles dealing with neuroimmunomodulation employ behavior as an analytical endpoint. Even fewer papers deal with social status as a possible modifier of neuroimmune phenomena. In the described sets of experiments, we tackle both, using a paradigm of social dominance and subordination. We first review data on the effects of different ranks within a stable hierarchical relationship. Submissive mice in this condition display more anxiety-like behaviors, have decreased innate immunity, and show a decreased resistance to implantation and development of melanoma metastases in their lungs. This suggests that even in a stable, social, hierarchical rank, submissive animals may be subjected to higher levels of stress, with putative biological relevance to host susceptibility to disease. Second, we review data on how dominant and submissive mice respond differentially to lipopolysaccharide (LPS), employing a motivational perspective to sickness behavior. Dominant animals display decreased number and frequency in several aspects of behavior, particularly agonistic social interaction, that is, directed toward the submissive cage mate. This was not observed in submissive mice that maintained the required behavior expected by its dominant mate. Expression of sickness behavior relies on motivational reorganization of priorities, which are different along different social ranks, leading to diverse outcomes. We suggest that in vitro assessment of neuroimmune phenomena can only be understood based on the behavioral context in which they occur. [ABSTRACT FROM AUTHOR]

Inflammation, particularly low-grade chronic inflammation, appears to affect several brain functions, from early brain development to the development of neurodegenerative disorders and perhaps some psychiatric diseases. On the other hand, nutrition and dietary components and patterns have a plethora of anti- and pro-inflammatory effects that could be linked to cognitive function. Even a modest effect of nutrition on cognitive decline could have significant implications for public health. This paper summarizes the available evidence regarding inflammation as a key mechanism in cognitive function and nutritional pro- or anti-inflammatory effects with the purpose of linking the apparent disparate disciplines of nutrition, immunity, and neurology. [ABSTRACT FROM AUTHOR]

Control of the acute phase of Trypanosoma cruzi infection is critically dependent on cytokine-mediated macrophage activation to intracellular killing, natural killer (NK) cells, CD4+ T cells, CD8+ T cells and B cells. Cell-mediated immunity in T. cruzi infection is also modulated by cytokines, but in addition to parasite-specific responses, autoimmunity can be also triggered. Importantly, cytokines may also play a role in the cell-mediated immunity of infected subjects. Here we studied the role of cytokines in the regulation of innate and adaptive immunity during the acute phase of T. cruzi infection in Wistar rats. Melatonin is an effective regulator of the immune system. Macrophages and T lymphocytes, which have melatonin receptors, are target cells for the immunomodulatory function of melatonin. In this paper melatonin was orally given via two protocols: prior to and concomitant with infection. Both treatments were highly effective against T. cruzi with enhanced action for the concomitant treatment. The data suggest an up-regulation of the TH-1 immune response as all analyzed parameters, interleukin (IL)-4, IL-10, transforming growth factor-β1 and splenocyte proliferation, displayed reduced levels as compared with the untreated counterparts. However, the direct effects of melatonin on immune cells have not been fully investigated during T. cruzi infection. We conclude that in light of the current results, melatonin exerted important therapeutic benefits through its immune regulatory effects. [ABSTRACT FROM AUTHOR]