کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2007118 1066364 2010 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
The absence of the VPAC2 receptor does not protect mice from Aspergillus induced allergic asthma
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
The absence of the VPAC2 receptor does not protect mice from Aspergillus induced allergic asthma
چکیده انگلیسی
Allergic asthma is a TH2-mediated disease marked by airway inflammation, increased mucus production, and elevated serum IgE in response to allergen provocation. Among its ascribed functions, the neuropeptide vasoactive intestinal peptide (VIP) is believed to promote a TH2 phenotype when signaling through its VPAC2 receptor. In this study, we assessed the requirement for the VIP/VPAC2 axis in initiating the allergic pulmonary phenotype in a murine model of fungal allergic asthma. C57BL/6 wild-type (WT) and VPAC2 knock-out (KO) mice were sensitized with Aspergillus fumigatus antigen and challenged with an aerosol of live conidia to induce allergic airways disease. WT and KO mice exhibited similar peribronchovascular inflammation, increased number of goblet cells, and elevated serum IgE. However, the absence of VPAC2 receptor resulted in a marked enhancement of MUC5AC mRNA with an associated increase in goblet cells and a reduction in eosinophils in the airway lumen at day 3 when VIP mRNA was undetectable in the KO lung. Sustained elevation of serum IgE was noted in KO mice at day 14, while the level in WT mice declined at this time point. These data suggest that the absence of VPAC2 does not protect mice from developing the signs and symptoms of allergic asthma.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Peptides - Volume 31, Issue 6, June 2010, Pages 1068-1075
نویسندگان
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