The aim of the present study was to investigate the association of the C allele of the CD14/-159 with phenotypes of atopy and asthma in an adult Dutch population in which linkage of total serum IgE and bronchial hyperresponsiveness to chromosome 5q31-33 is present.
A significant gene-gene interaction between S478P in IL4RA and the -1111 promoter variation in IL13, previously shown to be associated with BHR (P=.003), was detected.
B2AR polymorphisms may play an important role in the expression of nocturnal cough in atopic subjects but not in the expression of atopy and bronchial hyperresponsiveness in a general population.
De novo or augmented inhaled glucocorticoid therapy was associated with significant reductions in the percentages of CD4 T cells expressing IL-5 and IL-4 mRNA, as well as improvements in lung function, symptom scores, and bronchial hyperresponsiveness to metacholine (PD20) in both the atopic and nonatopic asthmatics.
De novo or augmented inhaled glucocorticoid therapy was associated with significant reductions in the percentages of CD4 T cells expressing IL-5 and IL-4 mRNA, as well as improvements in lung function, symptom scores, and bronchial hyperresponsiveness to metacholine (PD20) in both the atopic and nonatopic asthmatics.
A significant gene-gene interaction between S478P in IL4RA and the -1111 promoter variation in IL13, previously shown to be associated with BHR (P=.003), was detected.
The CTLA-4 promoter (-318 C/T) polymorphism was shown to be associated with asthma severity, but not with asthma, atopy, or bronchial hyperresponsiveness.
Significant association was also observed for the CTLA4-1147 C/T SNP with bronchial hyperresponsiveness (BHR) and asthma (P =.008 and.012, respectively), but not for allergy-related phenotypes.
The identification of ADAM33 as a major risk factor involved in the pathogenesis of BHR and airway wall remodelling provides insight into the pathogenesis of asthma and represents a novel therapeutic target.
Leukotrienes mediate murine bronchopulmonary hyperreactivity, inflammation, and part of mucosal metaplasia and tissue injury induced by recombinant murine interleukin-13.
Multivariate logistic regression analysis and nonparametric effect estimates (S-Plus) were applied to examine the association between endotoxin exposure and diagnosed asthma, related clinical symptoms, and bronchial hyperreactivity (BHR) stratified for noncarriers and carriers of G299/I399 polymorphism in the TLR4 gene.
The gene encoding CD14 is a positional candidate gene for allergic diseases as it is localized on chromosome 5q31.1, a region that is linked to asthma and bronchial hyperresponsiveness.
Polymorphisms of leukotriene C4 synthase did not determine responsiveness, in terms of attenuation of bronchial hyperresponsiveness, to leukotriene receptor antagonists in mild-to-moderate asthmatics.