Search

Anaphylaxis has rapidly spread around the world in the last several decades. Environmental factors seem to play a major role, and epigenetic marks, especially DNA methylation, get more attention. We discussed several GEO opening data classifications with TOP 100 specific methylation region values (normalized M-values on line) by machine learning, which are remarkable to classify specific anaphylaxis after monoallergen exposure. Then, we sequenced the whole-genome DNA methylation of six people (3 wormwood monoallergen atopic rhinitis patients and 3 normal-immune people) during the pollen season and analyzed the difference of the single nucleotide and DNA region. The results’ divergences were obvious (the differential single nucleotides were mostly distributed in nongene regions but the differential DNA regions of GWAS, on the other hand), which may have caused most single nucleotides to be concealed in the regions’ sequences. Therefore, we suggest that we should conduct more “pragmatic” and directly find special single-nucleotide changes after exposure to atopic allergens instead of complex correlativity. It is possible to try to use DNA methylation marks to accurately diagnose anaphylaxis and form a machine learning classification based on the single methylated CpGs.

Background While treatment for atopic rhinitis is aimed mostly to relieve symptoms, only allergen‐specific immunotherapy (AIT) is targeted to modify the natural history of allergic diseases. This results in sustained clinical tolerance, even when treatment has stopped. The immunomodulatory effects of AIT are attributed mainly to increased regulatory T‐cell function and increased allergen‐specific IgG4, yet little is known about the effect on the memory B‐cell compartment. Objective We aimed to examine the effects of AIT on the IgE‐ and IgG subclass‐expressing memory B cells. Methods We recruited 29 patients with atopic seasonal rhinoconjunctivitis and performed a longitudinal analysis of the peripheral immune compartment before, during, and after sublingual immunotherapy (SLIT) for allergy to temperate grass pollen, predominantly to ryegrass pollen (RGP; Lolium perenne). Using flow cytometry on peripheral blood mononuclear cells and serum immunoassays, we analyzed the effects of a 4 months preseasonal treatment regimen comprising two or three courses in consecutive years on circulating IgE+ and IgG+ memory B cells and allergen‐specific Ig levels. Results SLIT increased RGP‐specific serum IgG2 and IgG4, as well as the frequencies of IgG2 + and IgG4 + memory B cells, whereas no effect was observed on the IgE+ memory B‐cell compartment. Furthermore, SLIT enhanced proportions of regulatory T cells specific to RGP. These changes were associated with clinical improvement. Conclusion Our data provide evidence for immunological effects of SLIT on B‐cell memory. Skewing responses toward IgG2 and IgG4 subclasses might be a mechanism to suppress IgE‐mediated allergic responses., This study examines the effect of ryegrass pollen AIT on B‐cell responses in a population of 29 patients with allergic rhinitis. Successful immunotherapy for ryegrass pollen allergy increases allergen‐specific IgG2 and IgG4 serum levels, and proportions of IgG2‐ and IgG4‐expressing memory B cells. Skewing toward the anti‐inflammatory IgG2 and IgG4 subclasses might be a mechanism to suppress IgE‐mediated allergic responses.

In this commentary, we focus on allergy as a facilitating factor in the pathogenesis of alopecia areata (AA). From previous studies on AA, it is well known that subsets of patients can have one or more of; seasonal relapse, comorbid atopic rhinitis, asthma and dermatitis, lesion infiltrating eosinophils and plasma cells, high levels of total IgE, specific IgE for house dust mites (HDMs), and/or disrupted skin barrier function by the evaluation of filaggrin. Allergy and AA share a similar genetic background; both contributing to an immune reaction imbalance. Furthermore, adjunctive treatment with antihistamines, or desensitization for HDM, can reduce the severity of alopecia in atopic AA patients. Therefore, allergies may contribute to the onset and relapse of AA. Identification of an allergic or atopic immune component in AA patient subsets may indicate adjunctive treatment intervention measures against allergies should be taken which may improve the success of conventional AA treatment.

Allergic condition such as itching of the skin, or runny nose and sneezing are widely known, but different case of allergic reaction in the mouth. Are still unknown, one of them is Oral Allergy Syndrome (OAS). Almost everyone knows food allergens such as shrimp, or marine fish, but actually fresh fruits and vegetables also can trigger allergic reactions like OAS in the form of itching or swelling of the lips, tongue, palate, and pharynx. Author intends to provide further information about the OAS in this paper. The mechanism of OAS is a type I, immunoglobulin E-mediated hypersensitivity reaction, common in atopic people with history of atopic rhinitis, bronchial asthma, or urticaria. Food allergen that causes OAS have a cross reaction/ homolog with pollen from protein pathogen respons / PR-10 family, such as Bet v 1 (Birch) and Bet v 2 (Birch). Some OAS allergens from vegetables that homolog with Bet v 1 includes celery (Api g 1) and soybean (Gly m 4), and other allergens from fruits homolog with Bet v 2, such as Ana c1 alergen pineapple. The diagnosis of OAS based on medical history, clinical examination and diagnostic tests includes skin prick test, specific IgE serum, or basophil activation test, and cellular antigen stimulation test with an enzyme-linked immunosorbent assay. Management of OAS consists of non-pharmacological includes information and education to avoid the causes, and give suggestion to eat cooked food. Pharmacologically are prescription of antihistamines or epinephrine injection in case of emergencies. Signs and symptoms of OAS in fact have long been found, but its diagnosis and management are still not widely known. Dentist should know about signs and symptoms of food allergy in the oral mucosa include OAS which caused by fruits and vegetables such as celery, soybean, carrot, apple, pineapple, and strawberry, so finally dentist will provide good management for the patient..

The prevalence rate of allergic diseases, such as asthma, atopic rhinitis (AR), and atopic dermatitis (AD), has been significantly increasing over the years because of environmental changes. Type 2 immunity is mediated by allergic inflammation initiated by an innate immune response. This response is orchestrated by type 2 cytokines (interleukin [IL]-4, IL-5, IL-9, and IL-13) together with other cells. The dendritic cell [DC]-T helper 2 (Th2) cell axis is the conventional type 2 immune pathway, and is currently known as the group 2 innate lymphoid cell (ILC2)-DC-Th2 axis that mediates type 2 inflammation. ILC2s strongly mediate type 2 inflammation in allergic diseases. ILC2s are activated by epithelial cell-derived cytokines, such as IL-25 and IL-33, and thymic stromal lymphopoietin. Additionally, ILC2s are activated by mast cell lipid inflammatory mediators, such as cysteinyl leukotrienes and prostaglandin D2. ILC2s produce a large amount of type 2 cytokines. The important role of ILC2s in the pathogenesis of type 2-mediated disease has resulted in ILC2-derived cytokines being a target for therapeutic development. In this review, we discuss type 2 immunity, mainly the ILC2-DC-Th2 axis, and other immune cells, the dominant role of ILC2s in asthma, AR, and AD, and therapeutic targets against type 2 cytokines.

Background: Polymorphisms of cytokine genes are an interesting focus for association studies involving atopic diseases due to their role in immune cell communications during inflammation. The aim of this study was to investigate associations of TNFα -308G>A, TNFα -238G>A, IL-1α -889C>T and IL-10 -1082G>A polymorphisms with atopic diseases with adjustment for confounding lifestyle and environmental factors. Methods: This study was performed on 356 Croatian students. The diagnosis of atopic asthma, atopic rhinitis and atopic dermatitis was based on symptoms reported by the modified International Study of Asthma and Allergies in Childhood questionnaire and a positive skin prick test (SPT) to at least one common inhalatory allergen. Genetic polymorphisms were genotyped using the polymerase chain reaction-based technique. The influence of personal (gender, body mass index, parental history of atopic disease), lifestyle (cigarette smoking, pet ownership) and environmental (urban/rural residency, residency in continental/Mediterranean region) factors reported in the questionnaire was investigated by univariate and multivariate analysis. Results: Compared to the control subjects, univariate analysis showed a significant negative association of the TNFα -308G>A polymorphism with atopic asthma, atopic dermatitis, asthma and skin symptoms and positive SPT. These observations were confirmed in a multivariate model only for atopic dermatitis and skin symptoms (atopic dermatitis: OR = 0.27; 95% CI 0.07-1.00; p = 0.050; skin symptoms: OR = 0.29; 95% CI 0.10-0.83; p = 0.021). Conclusions: The results indicate a protective role of TNFα -308G>A genetic polymorphisms regarding atopic dermatitis and skin symptoms even after controlling for personal, lifestyle and environmental factors. Further studies are needed to elucidate the molecular patterns of this association in atopic dermatitis and other chronic inflammatory skin disorders.

The presentation of allergic diseases in children with autism spectrum disorder (ASD) was evaluated systematically through a literature search using MEDLINE, EMBASE, Cochrane Library, and CINAHL databases. Any comparative studies on children with ASD and allergic diseases were evaluated for eligibility followed by risk of bias assessment, data synthesis, and meta-analysis. No randomized clinical trials were identified but 10 eligible observational studies were found, all of low methodological quality. A high estimated prevalence of asthma (OR 1.69, 95 % CI 1.11 to 2.59; 2,191 ASD children) and atopic rhinitis (OR 1.66, 95 % CI 1.49 to 1.85; 1,973 ASD children) were indicated. Rates of food allergy did not show significant differences between groups. Currently, clinical evidence was not found to draw any specific clinical implication.

Thymic stromal lymphopoietin (TSLP) has been recently implicated as a key molecule for initiating allergic inflammation at the epithelial cell-dendritic cell (DC) interface. In humans, aberrant TSLP expression is observed in allergic tissues, such as lesional skins of atopic dermatitis, lungs of asthmatics, nasal mucosa of atopic rhinitis and nasal polyps, and ocular surface of allergic keratoconjunctivitis. TSLP is produced predominantly by damaged epithelial cells and stimulates myeloid DCs (mDCs). TSLP-activated mDCs can promote the differentiation of naive CD4+ T cells into a Th2 phenotype and the expansion of CD4+ Th2 memory cells in a unique manner dependent on OX40L, one of the tumor necrosis factor superfamily members with Th2-promoting function, and lack of production of IL-12. From a genetic point of view, multiple genome-wide association studies have repeatedly identified the TSLP gene as one of the loci associated with susceptibility to allergic diseases. Thus, TSLP is a rational therapeutic target for the treatment of allergic disorders. Elucidating the mechanisms that regulate TSLP expression and the effects of TSLP on orchestrating the immune response toward a Th2 phenotype is essential for developing anti-TSLP therapy.

There is conflicting evidence for the relationship between parental socioeconomic position and their children's asthma. The aim of this study was to investigate relationships between parental education and respiratory symptoms in their children, distinguishing atopic and non-atopic symptoms. A cross-sectional survey among 3262 elementary school children (age 8-13) was performed; data on parental education were obtained for 3213 children. Parents completed a questionnaire on their child's allergic and respiratory symptoms, and potential explanatory variables including family history, indoor environment, and the child's medical history. Subsets of children were tested for atopy (n = 1983), lung function (n = 2325), and airway hyperresponsiveness (AHR) (n = 880). Logistic regression was used to assess relationships of health outcomes with parental education. A high parental education was associated with an increased risk of atopic sensitization to indoor allergens (OR 1.31, 95% CI 1.02; 1.69). Studied explanatory variables did not influence the relationship. In contrast, a high parental education protected children from wheeze (OR 0.77, 95% CI 0.61; 0.97). This only applied to non-atopic wheeze (OR 0.65, 95% CI 0.43; 0.99) and not to atopic wheeze (OR 0.89, 95% CI 0.60; 1.31). The protection from non-atopic wheeze in children of highly educated parents declined after adjustment for household smoking and breastfeeding (OR 0.96, 95% CI 0.58; 1.57). Similar results were observed for non-atopic and atopic rhinitis. We conclude that children from highly educated parents are protected from non-atopic respiratory symptoms, which is largely explained by a lower rate of household smoking and a higher rate of breastfeeding.

There is conflicting evidence for the relationship between parental socioeconomic position and their children's asthma. The aim of this study was to investigate relationships between parental education and respiratory symptoms in their children, distinguishing atopic and non-atopic symptoms. A cross-sectional survey among 3262 elementary school children (age 8-13) was performed; data on parental education were obtained for 3213 children. Parents completed a questionnaire on their child's allergic and respiratory symptoms, and potential explanatory variables including family history, indoor environment, and the child's medical history. Subsets of children were tested for atopy (n = 1983), lung function (n = 2325), and airway hyperresponsiveness (AHR) (n = 880). Logistic regression was used to assess relationships of health outcomes with parental education. A high parental education was associated with an increased risk of atopic sensitization to indoor allergens (OR 1.31, 95% CI 1.02; 1.69). Studied explanatory variables did not influence the relationship. In contrast, a high parental education protected children from wheeze (OR 0.77, 95% CI 0.61; 0.97). This only applied to non-atopic wheeze (OR 0.65, 95% CI 0.43; 0.99) and not to atopic wheeze (OR 0.89, 95% CI 0.60; 1.31). The protection from non-atopic wheeze in children of highly educated parents declined after adjustment for household smoking and breastfeeding (OR 0.96, 95% CI 0.58; 1.57). Similar results were observed for non-atopic and atopic rhinitis. We conclude that children from highly educated parents are protected from non-atopic respiratory symptoms, which is largely explained by a lower rate of household smoking and a higher rate of breastfeeding.

Inflammation through the respiratory tract is a crucial event in immune disorders, including asthma, and atopic rhinitis. To investigate whether an aqueous extract of Angelica archangelica L. (AaL) has a beneficial influence in terms of anti-asthmatic activity, its effects on an ovalbumin-induced asthmatic model were examined. Mice sensitized to ovalbumin were orally administered the AaL extract, and their lungs examined by Haematoxylin-Eosin staining to determine IL-4/13 cytokine expression. The AaL extract exerted strong anti-asthmatic effects by regulating each level in the CD4? cell number, IL-4/13, and other target markers in the lungs. Together, these results collectively indicate that the aqueous AaL extract ameliorates asthmatic symptoms effectively in a mouse ovalbumin-challenge model.

Asthma, atopic dermatitis, and atopic rhinoconjunctivitis are three distinct conditions, which are characterized by the production of specific immunoglobulin E (IgE) against common, ubiquitous allergens such as house dust mites, pollen, or animal dander. Once sensitized, re-exposure to allergen induces an inflammatory reaction of the affected organ: the bronchial system, the nasal and ocular mucosa, or the skin, respectively. At present, atopic diseases are the most common chronic illnesses in children living in the industrialized world. In general, asthma and atopy rates are higher in affluent, Western countries with a high degree of industrialization than in developing countries with a large, rural population. In a worldwide study in approximately 500,000 school-aged children from 56 countries, the highest prevalence of asthma was found in the United Kingdom, New Zealand, and Australia, and most developing countries had comparatively low prevalence rates. Within European countries, a West–East gradient in the prevalence of childhood asthma is present, which became apparent in studies shortly after the fall of the communist East. In the Baltic area of Northern Europe, Swedish children had a higher prevalence of atopic sensitization and asthma than did those from Poland and Estonia [1, 2]. Likewise, the prevalence of asthma, allergic rhinitis, and atopic sensitization was significantly higher in West Germany than in the East [3], a genetically homogeneous study population that had lived under very different economic and environmental circumstances for 40 years. In the years since unification, however, atopic sensitization as well as atopic rhinitis have increased significantly in East German children, almost to levels found in Western Germany, and levels of asthma were still low [4]. As most children in the communist system grew up in day-care centers from an early age, an intriguing explanation for these findings was that the early exposures to infections and microbial matter in day-care centers may have influenced the susceptibility to atopic diseases.

In clinically stable asthma the exhaled NO values (F(E)NO) are generally higher than in control subjects. Therefore, reference values are of limited importance in clinical practice. This is demonstrated in this case report, but it is also shown that NO parameters from non-linear modelling do have a clinical value. A subject with asthma was treated with inhaled corticosteroids for 1 week. The non-linear NO model was used to measure the response to treatment. The NO parameters from subjects with atopic rhinitis and asthma were fed into a computer program to generate theoretical F(E)NO₀.₀₅ values, i.e. target values. There was a dramatic decrease in F(E)NO₀.₀₅ due to treatment, from 82 to 34 ppb, but it remained higher than in healthy controls. This is due to the elevated diffusion rate of NO, unchanged by treatment. When the NO parameters are known, a personal best value of F(E)NO₀.₀₅ (fractional concentration of exhaled NO in the gas phase, 0.05 L/s) can be calculated, which can be the target value when only F(E)NO₀.₀₅ can be monitored. In conclusion, reference values for NO parameters are shown to be clinically useful. It is essential that every patient receives his/her target value of F(E)NO₀.₀₅, when only a single NO measurement is available. In our opinion, this is the reason why there are few successful studies of trying to target the NO value with inhaled corticosteroids.

Decreased spirometric indices are characteristic of asthma and other respiratory diseases. The aim of this study was to investigate the genetic and environmental components of variance of forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) measured in adulthood in an Australian population-based sample of 468 Caucasian nuclear families. The inter-relationships of the genetic determinants of these traits with asthma and atopic rhinitis were also investigated.Serial cross-sectional studies were conducted in the town of Busselton in Western Australia between 1966 and 1981 and follow-up of previous attendees was undertaken in 1995. Data from each subject included in this study were from a single survey in adulthood (25–60 yrs of age) when the subject was as close to age 45 yrs as possible.Multivariate analysis suggested that FEV1and FVC levels were associated with age, sex, height, tobacco smoke exposure, asthma and atopic rhinitis. After adjustment for relevant covariates, FEV1levels had a narrow-sense heritability (h2N) of 38.9% (SE 9.1 %). FVC levels had anh2Nof 40.6% (SE 8.9%). Extended modelling demonstrated little overlap in the genetic determinants of asthma or atopic rhinitis and either FEV1or FVC levels.The results of this study were consistent with the existence of important genetic determinants of adult lung function that are independent of asthma or other atopic disease, cigarette smoking, height, age or sex.

Background Obesity is regarded as a potential risk factor for atopy. The aim of this study was to assess the associations of obesity with atopic dermatitis, rhinitis, asthma and food allergy in Chinese adults. Methods Two hundred and sixty six (266) atopic cases in Harbin, China, were identified according to the current Chinese guidelines for the diagnosis of atopic diseases. All cases had a previous diagnosis of atopic disorders (atopic dermatitis, rhinitis, asthma or food allergy) and were positive in one or more allergen specific IgE tests to 16 common allergens in the region. Each case was individually matched to two healthy controls based on their age, sex, and residential regions. All 532 healthy controls were negative in allergen specific IgE tests. The associations of obesity with four atopic disorders were assessed using a conditional logistic regression method. Results Obesity was significantly associated with the presence of atopic diseases (OR = 3.2, 95% CI: 1.8, 5.7). Males and females had a similar association (OR = 3.1 for males and 3.2 for females). The associations of obesity with atopic dermatitis (OR = 2.7, 95% CI: 1.2, 6.3) and atopic rhinitis (OR = 3.1, 95% CI: 1.1, 8.7) were statistically significant. Although obesity was positively associated with atopic asthma, this association was not statistically significant (OR = 3.4, 95% CI: 0.6, 19.9). The association between obesity and food allergy was weak and not significant (OR = 1.1, 95% CI: 0.4, 3.7). Conclusions Obesity is positively associated with the presence of atopic diseases in Chinese adults. Specifically, obesity is significantly associated with atopic dermatitis and rhinitis. Our findings warrant further investigation on the causal nature between obesity and atopic diseases and the effect of weight reduction on preventing atopic diseases.

Crosslinking of immunoglobulin E antibodies (IgE) bound at the surface of mast cells and subsequent mediator release is considered the most important trigger for allergic reactions. Therefore, the genetic control of IgE levels is studied in the context of allergic diseases, such as asthma, atopic rhinitis, or atopic dermatitis (AD). We performed genome-wide association studies in 161 Labrador Retrievers with regard to total and allergen-specific immunoglobulin E (IgE) levels. We identified a genome-wide significant association on CFA 5 with the antigen-specific IgE responsiveness to Acarus siro. We detected a second genome-wide significant association with respect to the antigen-specific IgE responsiveness to Tyrophagus putrescentiae at a different locus on chromosome 5. A. siro and T. putrescentiae both belong to the family Acaridae and represent so-called storage or forage mites. These forage mites are discussed as major allergen sources in canine AD. No obvious candidate gene for the regulation of IgE levels is located under the two association signals. Therefore our studies offer a chance of identifying a novel mechanism controlling the host's IgE response.

Inflammation of the respiratory tract is a crucial process in immune diseases, including asthma, and atopic rhinitis. To establish whether an aqueous extract of Spinacia oleracea Linn (SoL) has a beneficial influence in terms of antiasthmatic activity, we examined its effects on an ovalbumin-induced asthmatic model. Mice sensitized to ovalbumin were orally administered the SoL extract, and their lungs examined by hematoxylin and eosin staining to determine IL-4/13 cytokine expression. The SoL extract exerted strong antiasthmatic effects by inducing a decrease in the CD4 + cell number, IL-4/13, and other molecular markers in the lung. Our results collectively indicate that the aqueous SoL extract ameliorates asthmatic symptoms effectively in a mouse ovalbumin-challenge model.

There is conflicting evidence for the relationship between parental socioeconomic position and their children's asthma. The aim of this study was to investigate relationships between parental education and respiratory symptoms in their children, distinguishing atopic and non-atopic symptoms. A cross-sectional survey among 3262 elementary school children (age 8-13) was performed; data on parental education were obtained for 3213 children. Parents completed a questionnaire on their child's allergic and respiratory symptoms, and potential explanatory variables including family history, indoor environment, and the child's medical history. Subsets of children were tested for atopy (n = 1983), lung function (n = 2325), and airway hyperresponsiveness (AHR) (n = 880). Logistic regression was used to assess relationships of health outcomes with parental education. A high parental education was associated with an increased risk of atopic sensitization to indoor allergens (OR 1.31, 95% CI 1.02; 1.69). Studied explanatory variables did not influence the relationship. In contrast, a high parental education protected children from wheeze (OR 0.77, 95% CI 0.61; 0.97). This only applied to non-atopic wheeze (OR 0.65, 95% CI 0.43; 0.99) and not to atopic wheeze (OR 0.89, 95% CI 0.60; 1.31). The protection from non-atopic wheeze in children of highly educated parents declined after adjustment for household smoking and breastfeeding (OR 0.96, 95% CI 0.58; 1.57). Similar results were observed for non-atopic and atopic rhinitis. We conclude that children from highly educated parents are protected from non-atopic respiratory symptoms, which is largely explained by a lower rate of household smoking and a higher rate of breastfeeding.

Background: The interleukin (IL) 4/IL13 pathway is involved in the regulation of IgE production associated with atopic diseases. Numerous polymorphisms have been identified in the coding region of the IL4 receptor α chain (IL4Ra) and previous association studies have shown conflicting results. Based on their putative functional role, polymorphisms A148G, T1432C and A1652G, located in the coding region of IL4Ra, were selected for association and haplotype studies in a large German population sample (n = 1,120). Methods: Genotyping was performed using allele-specific PCR and restriction-enzyme-based assays. Haplotypes were estimated, and population-derived IgE percentiles (50% IgE >60 IU/ml, 66% IgE >115 IU/ml and 90% IgE >457 IU/ml) were calculated as outcome variables in a haplotype trend regression analysis. Results: In our population, only polymorphism T1432C showed a trend for a protective effect against atopic rhinitis (odds ratio, OR: 0.52, 95% confidence interval, CI: 0.26–1.02, p = 0.05). When haplotypes were calculated, one haplotype was significantly associated with elevated serum IgE levels at the 50th percentile (OR 1.60, 95% CI 1.08–2.37, p = 0.02). Conclusions: These data indicate that IL4Ra polymorphisms, although suggested to be functionally relevant by in vitro studies, have only a minor influence on IgE regulation in our large population sample.

Background: A high prevalence of bronchial hyperresponsiveness (BHR) was found in atopic subjects with rhinitis. Those subjects may be at higher risk for developing bronchial asthma. We evaluated, in a 7-year follow-up, BHR and atopy in a homogeneous population of nonasthmatic children with allergic rhinitis (AR), and their role in asthma development. Methods: Twenty-eight children (6–15 years) with AR were studied. At enrollment (T0), skin tests, total serum IgE assay, peak expiratory flow (PEF) monitoring and methacholine (Mch) bronchial challenge were performed. BHR was computed as the Mch dose causing a 20% forced expiratory volume (FEV)1 fall (PD20FEV1) and as dose–response slope (DRS). Subjects were reassessed after 7 years (T1) using the same criteria. Results: At T0, 13 children (46%), showing a PD20FEV1

Aims-To investigate the ability of circulating IgG autoanti-IgE antibodies from atopic rhinitis patients to block the binding of IgE to its low affinity receptor (FcepsilonRII), also termed CD23.Methods-This involved the use of a well validated flow cytometric method to detect inhibition of FITC labelled IgE binding to human B cells expressing CD23 (RPMI 8866 cell line).Results-Taking inhibition values greater than 20% as being significant, 15 out of 20 IgG anti-IgE containing sera inhibited the binding of IgE-FITC to the RPMI 8866 cells. The inhibitory effect was recoverable in the IgG fraction of serum, but was not related to the titre of either IgG1 anti-IgE or IgG4 anti-IgE, thus suggesting that it might be related to epitope specificity. No such inhibition was demonstrable with rheumatoid sera containing autoanti-IgG (that is, rheumatoid factor), but lacking autoanti-IgE.Conclusions-The capacity of anti-IgE to block the binding of IgE to CD23 has important implications, particularly in terms of upregulation of IgE synthesis and the consequent perpetuation of the inflammatory response.

Chemokines and their receptors play an important role in the late inflammatory stage of asthma. In this study, we aimed to investigate polymorphisms of MCP-1 (CCL2), CCR2 and CCR5 which can affect qualitatively and/or quantitatively their production and thus influence both susceptibility and severity of asthma and its clinical and biological features. MCP-1 (A/G -2518), CCR2 (+/64I), CCR5 (G/A -59029) and CCR5 (032) polymorphisms were evaluated by PCR in 107 Tunisian patients with asthma and 169 healthy controls. No significant association was found between the four investigated polymorphisms and asthma. Nevertheless the haplotype MCP1*AG /CCR2*+/+ was significantly l ess frequent in patients (20.5%) compared to controls (32.5%) (p=0.03; OR=0.54; 95% CI: 0.29-0.98). Whereas no difference was observed in CCR2/CCR5 haplotypes between patients and controls. Analysis of polymorphisms with clinical and biological features showed that the concomitant presence of MCP-1*G/CCR2*64I alleles was less frequent in severe forms (4.34%) compared to moderate disease (12%) but the difference was not significant (p=0.27). No association was observed between the four polymorphisms and the presence of atopic rhinitis or atopic conjunctivitis and an elevated rate of serum IgE over 200 IU/ml. Additional effects of MCP-1 and its receptor CCR2 polymorphisms seem to be involved in disease susceptibility to asthma in Tunisian patients; nevertheless they could be protective against its severe forms.

1.Three cases of Loeffler's syndrome are discussed. In each instance, atopic rhinitis and asthma were present and sensitivities to multiple inhalant allergens were demonstrated. 2.Presumably, polyvalent bacterial or intrinsic sensitivities were present in all three patients in addition to recognized extrinsic sensitivities. It is difficult and often impossible in the presence of multiple sensitivities to incriminate any single antigen as the cause of an episode of allergic pulmonary infiltration. 3.In two of the patients described, pulmonary infiltrations were characteristically transitory. In the third patient, although early infiltrations were of fleeting character, repeated attacks have left increasing residual fibrosis and evidence of irreversible damage. It is believed that irreversible changes after allergic pulmonary infiltrations are especially apt to occur when so-called intrinsic or bacterial sensitivities are present.

Allergic diseases, such as atopic rhinitis, bronchial asthma and urticaria, are prevalent and increasing in frequency. Mast cells are known to play a central role in the immediate phase reaction of allergic diseases through the IgE-mediated release of a variety of chemical mediators, such as histamine, leukotrienes and prostaglandins. In contrast, T lymphocytes, basophils and eosinophils are thought to be responsible for inducing the late phase response. However, whether the mast cell can be simplistically assigned a role in the immediate phase allergic response and whether mast cells are necessary for the ongoing allergic response, including the development of hyperresponsiveness, remains to be completely studied. In the present article, the author will discuss the integrated roles of mast cells in IgE-mediated allergic inflammation, with specific emphasis on the roles of mast cell-derived cytokines in the late phase allergic response and chronic allergic inflammation.