Low Interleukin 10 Production at Birth Is a Risk Factor for Atopic Dermatitis in Neonates with Bifidobacterium Colonization.

BACKGROUND: Altered regulatory immune responses to microbial stimuli and intestinal colonization of beneficial bacteria early in life may contribute to the development of allergic diseases (e.g., atopic dermatitis [AD]). However, few reports have investigated these factors simultaneously. The purpose of this study was to analyze neonatal immune responses to microbial stimuli as well as intestinal colonization of beneficial bacteria, in relation to the development of AD in a birth cohort. METHODS: Pregnant women were recruited, and their infants were followed up until 7 months of age. Levels of interleukin (IL)-10 released from cord-blood mononuclear cells (CBMCs) stimulated with heat-killed gram-positive bacteria (Bifidobacterium bifidum and Lactobacillus rhamnosus GG) and Lactobacillus-derived peptidoglycan were measured. Fecal Bifidobacterium counts at 4 days and 1 month were quantified using real-time polymerase chain reaction. The development of AD was determined by means of a questionnaire at 7 months of age. RESULTS: The levels of released IL-10 were significantly lower in infants with AD (n = 17) than in infants without AD (n = 53) for all stimuli. In infants with fecal Bifidobacterium, the incidence of AD was inversely associated with the release of IL-10 from cord blood mononuclear cells. CONCLUSION: Our findings suggest that impaired IL-10 production in response to microbial stimuli at birth may be associated with an increased risk of developing infantile AD, even in infants with early colonization of intestinal bifidobacteria.

T helper lymphocyte response to respiratory syncytial virus and its components in patients with respiratory allergy and nonatopic controls.

BACKGROUND: Respiratory syncytial virus (RSV) G protein is involved in Th2-shifted immune response, while F protein has a reverse effect on RSV infection in Th2-prone BALB/c mice. Studies on the human T cell response to F or G protein are few, and the relationship between the immune response to G protein and atopy is not known. METHODS: We established CD4+ RSV-specific T cell lines (TCLs) from adult patients with respiratory allergic diseases (allergics) or nonatopic controls (controls), and examined proliferative responses and gamma-interferon (IFN-gamma) and interleukin 4 (IL-4) production in these TCLs upon stimulation with RSV, F or G proteins. RESULTS: 32 and 29 RSV-specific oligoclonal TCLs were established from allergics and controls, respectively. IL-4/IFN-gamma in the culture supernatant of antigen-stimulated TCLs was significantly higher in allergics than in controls (p = 0.042). IL-4/IFN-gamma ratios in the culture supernatants of G-protein-reactive TCLs were significantly higher in allergics than in controls (p = 0.016), while no differences in IL-4/IFN-gamma in culture supernatants of F-protein-reactive TCLs were found between allergics and controls (p = 0.787). IL-4/IFN-gamma in the culture supernatants of G-protein-reactive TCLs was significantly higher than those of F-protein-reactive TCLs in allergics (p = 0.023) but not in controls (p = 0.768). CONCLUSION: The results suggest that the T cell response to RSV is influenced by the atopic diathesis as well as by individual RSV antigens, and that G protein may be an important antigen involved in allergy in humans.