Search

Background: The aetiology of food allergy remains unclear. Although failure to develop or breakdown in oral tolerance has been proposed, the existence of physiologic sensitization routes other than the gastrointestinal tract cannot be excluded., Objective: The purpose of this study is to clarify whether or not exposure to allergen through the skin can promote food allergy., Methods: BALB/c mice were shaved on the back, and a patch impregnated with 100 micro g of ovalbumin (OVA) was applied to the dorsal skin for a 1-week period and then removed. After three courses of sensitization, OVA-specific antibodies in sera were measured, and then mice were orally challenged with 50 mg of OVA. Anaphylactic symptoms, plasma histamine levels, and histology of intestines and lungs after oral challenge were examined., Results: Epicutaneous (EC) sensitization of mice to OVA induced a high level of OVA-specific IgE. Subsequent oral challenge with OVA resulted in symptoms of systemic anaphylaxis with elevated levels of plasma histamine as well as histological changes in both intestines and lungs. In the presence of anti-IL-4 antibodies, EC sensitization failed to provoke an IgE response, but still induced a Th2-predominant cellular immune response in lungs after oral challenge., Conclusion: We demonstrated for the first time that food allergy can be induced by allergen exposure through the skin. Our results identify a novel role of EC sensitization in the pathogenesis of food allergy.

Background: House dust mite (HDM) Dermatophagoides pteronyssinus is the most important source of indoor allergens that cause allergic diseases in Taiwan. We prepared purified HDM allergens (Der p 1, Der p 2 and Der p 5) to detect allergen-specific immunoglobulin (Ig) E responsiveness among a large number of test subjects. The robust genetic typing system for HLA class II genes also facilitated the study on association of HLA and allergic response toward HDM., Objective: This study intended to investigate the association between HLA class II alleles and the IgE responsiveness to the major allergens from HDM, D. pteronyssinus., Methods: Two hundred and forty-eight subjects were selected for HLA association study. Plasma HDM allergen (Der p 1, Der p 2, Der p 5) -specific IgE and Der p 2-specific IgG antibodies were detected by ELISA, while HLA class II -DRB1, -DQA1, -DQB1, -DPB1 genetic polymorphism was determined by polymerase chain reaction/sequence-specific oligonucleotide probe hybridization (PCR/SSOPH). Statistical comparison of the allelic distribution of each HLA class II genes among the individuals with/without HDM allergen-specific IgE and IgG antibodies were performed., Results: There was no significant association between HLA DRB1, DQB1, DQA1 alleles and HDM-specific IgE responsiveness noted. Only DRB1*0803 and the linked DQA1*0103 alleles showed positive association with Der p 5-specific IgE responsiveness. However, we found that HLA-DPB1*1301 predisposed subjects to IgE responsiveness to HDM Der p 5. HLA DPB1*0501 was weakly associated with the IgE responsiveness to HDM Der p 1 and Der p 5. There was a strong negative association between the HLA-DPB1*0201 allele with IgE responsiveness to Der p 1 (OR: 0.30, P

Background and Objective: Repeated exposure of aerosolized antigen via respiratory tract can induce immunoglobulin (Ig) E isotype-specific tolerance to this antigen. However, the atopic individuals often produce a higher titre of IgE in response to airborne environmental allergens. The mechanisms of this differential regulation of airway allergen-specific immune responses are not fully understood. This study investigated the role of airborne endotoxin on the initiation of antigen-specific airway allergic responses., Methods: ELISA methods for detection of isotypes of antigen-specific antibodies and competitive reverse transcription polymerase chain reaction for detection mRNA of cytokines were used. In addition, Liu stain method was used to analyse the amounts of eosinophils in bronchoalveolar lavage fluid., Results: Mice pre-exposed with airborne endotoxin mounted significantly higher amounts of OVA-specific IgE antibody responses to inhaled OVA than those OVA-only sensitized mice. Inhaled endotoxin could downregulate repeated airway antigen exposure-induced IgE isotype-specific tolerance and increase antigen-induced lung eosinophils infiltration., Conclusions: These data show that airborne endotoxin exposure could potentiate allergen-specific airway inflammation. The results should have potential implications for understanding the development of allergen-induced airway allergic responses.

Repeated inhalation of allergen leads to the down-regulation of allergen-specific IgE responses in non-atopic individuals as well as in mice. This phenomenon is named inhalation-induced IgE tolerance. In contrast, inhaled allergen causes significant IgE and allergic responses in atopic persons. The mechanisms involved in this differential regulation of airway allergen-specific immune responses remain unclear. Besides the allergen exposure of genetically susceptible individuals, environmental contamination is considered to play a role as an initiating factor for airway allergic responses. Using a murine model, we demonstrate here that airborne beta-1, 3-D-glucan, which exists frequently in our environment, particularly in highly humid areas, can abrogate inhalation-induced IgE isotype-specific down-regulation and promote airway eosinophil infiltration to inhaled antigen.

We used allergen-specific ELISA to evaluate environmental distributions of house dust mite allergens (Der p I and Der p V) in the homes of 46 asthmatic, 20 atopic, and 26 nonatopic control children during the summer and winter. Geometric mean Der p I levels were approximately 10 times higher than geometric mean Der p V concentrations. The concentrations of Der p I and Der p V in winter were significantly higher than concentrations found in summer. In addition, we found no differences in Der p I concentrations among the three groups in summer; however, in winter, Der p I levels in the control group were significantly higher than levels in the homes of both asthmatic and atopic children. During the summer, concentrations of Der p V were lower in the control group, compared with the asthmatic group, but during the winter, concentrations in the control group were higher than levels found in either asthmatic or atopic children's homes. In this study, we did not establish an important relationship between mite allergen exposure and atopy/asthma.