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Glycoprotein 2 (GP2) is a widely distributed protein in the digestive tract, contributing to mucosal barrier maintenance, immune homeostasis, and antigen-specific immune response, while also being linked to inflammatory bowel disease (IBD) pathogenesis. This review sheds light on the extensive distribution of GP2 within the gastrointestinal tract and its intricate interplay with the immune system. Furthermore, the significance of GP2 autoantibodies in diagnosing and categorizing IBD is underscored, alongside the promising therapeutic avenues for modulating GP2 to regulate immunity and maintain mucosal balance.

Probiotics have emerged as agents that improve a wide range of conditions and provide essential ingredients for potential health benefits. Probiotics exhibit a diverse array of effects by engaging in [...]

The close phylogenetic relationship between humans and great apes results in similarities in infection susceptibility and a high potential for pathogen exchange (2,2). Despite this zoonotic potential, previous studies of [...]

Background: Offspring consistently exhibit similar imaging features as their parents in cases of degenerative lumbar scoliosis (DLS). Nevertheless, the role of genetic factors in the pathogenesis of DLS remains uncertain. Methods: A prospective analysis was conducted on 35 patients with DLS and their 36 offspring. Genomic DNA was extracted from 71 blood samples for gene mutation analysis using whole exome sequencin. Various demographic and imaging parameters were compared. Results: In 11 pedigrees of the 35 family members with DLS, 13 suspected pathogenic genes were identified. Among the 35 DLS patients, 11/35(31.5%) exhibited susceptibility gene mutations (mutant group), while 24/35(68.5%) had no pathogenic gene mutations (non-mutant group). AVR was more severe in mutant group than that in no-mutant group (p < 0.05). Among the 36 offspring, 11/36(30.6%) cohorts presented susceptibility genes (mutant group), 25/36(69.4%) cohorts presented no pathogenic genes (no-mutant group). More cohorts in the mutant group presented vertebral rotation (72.8%) and scoliosis (45.5%) than those (24%), (12%) in the no-mutant group, respectively (p < 0.05). Among the 36 offspring, 8/36(22.2%) presented scoliosis (study group), they all presented the same scoliosis orientation and apex vertebrae/disc location to their parents, the other 28/36(77.8%) cohorts without scoliosis were enrolled as control group, the mutation rate (62.5%) was higher in study group than that (21.4%) in control group. Conclusions: Genetic influences are significant in the onset of DLS, with affected families showing similar scoliosis patterns and identical apex vertebrae. Moreover, individuals with genetic mutations tend to have more pronounced vertebral rotation and at a higher risk of developing scoliosis. [ABSTRACT FROM AUTHOR]

Background Objective Methods Results Conclusions Eczema and psoriasis are common diseases. Despite both showing active epidermal contribution to the inflammatory process, their molecular aetiology and pathological mechanisms are different.Further molecular insight into these differences is therefore needed to enable effective future diagnostic and treatment strategies. The majority of our mechanistic and clinical understanding of psoriasis and eczema is derived from RNA, immunohistology and whole skin biopsy data.In this study, non‐invasive epidermal sampling of lesional, perilesional and non‐lesional skin from diseased and healthy skin was used to perform an in depth proteomic analysis of epidermal proteins.Our findings confirmed the psoriasis‐associated cytokine IL‐36γ as an excellent protein biomarker for lesional psoriasis. However, ELISA and ROC curve analysis of 53 psoriasis and 42 eczema derived samples showed that the sensitivity and specificity were outperformed by elastase‐specific protease inhibitor, elafin. Of note, elafin was also found upregulated in non‐lesional psoriatic skin at non‐predilection sites demonstrating inherent differences between the non‐involved skin of healthy and psoriatic individuals. Mass spectrometry and ELISA analysis also demonstrated the upregulation of the anti‐inflammatory molecule IL‐37 in psoriatic perilesional but not lesional skin. The high expression of IL‐37 surrounding psoriatic plaque may contribute to the sharp demarcation of inflammatory morphology changes observed in psoriasis. This finding was also specific for psoriasis and not seen in atopic dermatitis or autoimmune blistering perilesional skin. Our results confirm IL‐36γ and add elafin as robust, hallmark molecules distinguishing psoriasis and eczema‐associated inflammation even in patients under systemic treatment.Overall, these findings highlight the potential of epidermal non‐invasive sampling and proteomic analysis to increase our diagnostic and pathophysiologic understanding of skin diseases. Moreover, the identification of molecular differences in healthy‐looking skin between patients and healthy controls highlights potential disease susceptibility markers and proteins involved in the initial stages of disease. [ABSTRACT FROM AUTHOR]

Background: Epilepsy is associated with the immune system and metabolism; however, its etiology remains insufficiently understood. Here, we aim to elucidate whether circulating immune cell profiles and metabolites impact the susceptibility to epilepsy. Methods: We used publicly available genetic data and two-sample Mendelian randomization (MR) analyses to establish causal relationships and mediating effects between 731 immune cells and 1,400 metabolites associated with epilepsy. Sensitivity analyses were conducted to detect heterogeneity and horizontal pleiotropy in the study results. Results: MR analysis examining the relationship between immune cells, metabolites, and epilepsy revealed significant causal associations with 28 different subtypes of immune cells and 14 metabolites. Besides, the mediation effects analysis revealed that eight metabolites mediated the effects of six types of immune cells on epilepsy and that 3-hydroxyoctanoylcarnitine (2) levels exhibited the highest mediating effect, mediating 15.3% (95%CI, -0.008, -30.6%, p = 0.049) of the effect of DN (CD4-CD8-) AC on epilepsy. 1-(1-enylstearoyl)- 2-linoleoyl-GPE (p-18:0/18:2) levels (95%CI, 0.668, 10.6%, p = 0.026) and X-12544 levels (95%CI, -15.1, -0.856%, p = 0.028) contributed 5.63 and 8%, respectively, to the causal effect of FSC-A on myeloid DC on epilepsy. Conclusion: This study revealed a significant causal link between immune cells, metabolites, and epilepsy. It remarkably enhances our understanding of the interplay between immune responses, metabolites, and epilepsy risk, providing insights into the development of therapeutic strategies from both immune and metabolic perspectives. [ABSTRACT FROM AUTHOR]

Soybean is one of the most economically important crops worldwide. However, soybean yield can be substantially decreased by many diseases. Soybean genotypes could have different reactions to pathogen infection. As a first step toward investigating the biochemical basis of soybean resistance and susceptibility to disease, phytochemicals in the seeds of 52 soybean genotypes previously reported to have different reactions to diseases of soybean rust (SBR), Phomopsis seed decay (PSD), and purple seed stain (PSS) were analyzed. Using GC-MS, a total of 46 compounds were tentatively identified which included 11 chemical groups. Among those, the major group was esters, followed by carboxylic acid, ketone, and sugar moieties. Compounds having reported antioxidant, anti-microbial, and anti-inflammatory activities were also identified. UHPLC-DAD/MS analysis indicated that there were five major isoflavone components presented in the samples, including daidzin, glycitin, genistin, malonyldaidzin, and malonylglycitin. Isoflavones have been reported to play an important role in defense from plant pathogens. Although there was variance in the isoflavone content among soybean genotypes, those with the SBR resistance Rpp6 gene (PI 567102B, PI 567104B, PI 567129) consistently exhibited the highest concentrations of daidzin, glycitin, genistin, and malonyldaidzin. The SBR resistant genotype, PI 230970 (Rpp2) had the greatest amount of genistin. The SBR resistant genotype, PI 200456 (Rpp5) resistant genotype uniquely contained glycitein, a compound that was absent in the other 51 genotypes examined. A PSD-resistant genotype PI 424324B had nearly four times the amount of stigmasterol as PI 556625, which was susceptible to SBR, PSD, and PSS in our previous tests. Results of this study provide useful information for further investigation of the biochemical basis of soybean resistance to diseases. The results may also aid in selection of soybean lines for breeding for resistance to soybean rust and other diseases. [ABSTRACT FROM AUTHOR]

The intricate interplay between cellular senescence and alterations in the gut microbiome emerges as a pivotal axis in the aging process, increasingly recognized for its contribution to systemic inflammation, physiological decline, and predisposition to age‐associated diseases. Cellular senescence, characterized by a cessation of cell division in response to various stressors, induces morphological and functional changes within tissues. The complexity and heterogeneity of senescent cells, alongside the secretion of senescence‐associated secretory phenotype, exacerbate the aging process through pro‐inflammatory pathways and influence the microenvironment and immune system. Concurrently, aging‐associated changes in gut microbiome diversity and composition contribute to dysbiosis, further exacerbating systemic inflammation and undermining the integrity of various bodily functions. This review encapsulates the burgeoning research on the reciprocal relationship between cellular senescence and gut dysbiosis, highlighting their collective impact on age‐related musculoskeletal diseases, including osteoporosis, sarcopenia, and osteoarthritis. It also explores the potential of modulating the gut microbiome and targeting cellular senescence as innovative strategies for healthy aging and mitigating the progression of aging‐related conditions. By exploring targeted interventions, including the development of senotherapeutic drugs and probiotic therapies, this review aims to shed light on novel therapeutic avenues. These strategies leverage the connection between cellular senescence and gut microbiome alterations to advance aging research and development of interventions aimed at extending health span and improving the quality of life in the older population. [ABSTRACT FROM AUTHOR]

AbstractSex plays a crucial role in shaping the immune response of vertebrates, leading to differing susceptibilities to diseases between females and males. This review explores the observed sexually dimorphic patterns in different pathogenic infections, immune responses, and molecular events. First, a compilation of historical guidelines for incorporating gender/sex as a variable in research studies to enhance scientific rigor, improve research outcomes, and promote better health for both sexes has been carried out. Following this, the study focuses on examining sex-based differences in immune responses across different taxa, with an in-depth review of available studies on fish, particularly regarding the prevalence of sex-related differences in parasites, viruses, and bacteria. Furthermore, the benefits of considering sexual dimorphism when evaluating the prevalence of diseases in fish management in aquaculture and ecological contexts have been discussed. Integrating sex in understanding immune responses will positively influence fish welfare, economic impacts, and policymaking, leading to more tailored and effective treatments. [ABSTRACT FROM AUTHOR]