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- W2286611921 abstract "Abstract Genes relevant to allergic lung disease were re-evaluated using our fungal inhalation model. We focused on the asthma phenotype as well as fungal clearance in IL-13, IL-5, Stat6, Rag1, CD1, and TSLP deficient mice. For asthma phenotyping, genetic knock-out (or anti-IL-5 treated) mice were intra-nasally inoculated with 400,000 Aspergillus niger conidia every other day for 16 days, and endpoints measured 24 hours after the final dose. The endpoints measured were airway hyper-reactivity (AHR), bronchial lavage fluid differential cell analysis, and lung IL-4 and IFNγ elispot analysis. For fungal clearance, mice were intra-nasally inoculated with 400,000 Aspergillus niger conidia, and lungs removed at various time points to determine the number of viable conidia remaining. Our results confirmed the requirement of IL-13, Stat6, Rag1, and TSLP for AHR induction; the requirement of Stat6, Rag1, IL-13, IL-5 and TSLP for eosinophil recruitment; the requirement of IL-13, Stat6, Rag1, and TSLP for IL-4 producing cells recruitment. CD1 KO mice showed an exaggerated phenotype with increased AHR and IL-4 production. IL-13, Rag1, and IL-5 were required for optimal fungal clearance. Thus, similar to non-infectious asthma models, conventional T cells, the IL-13 signaling pathway and TSLP were important for disease expression induced by viable fungi. In contrast, non-conventional CD1-resrticted NKT cells were found to be potent suppressors of fungal-dependent allergic lung disease." @default.
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- W2286611921 date "2010-04-01" @default.
- W2286611921 modified "2023-09-23" @default.
- W2286611921 title "Reassessment of innate and adaptive immune pathways in fungal-dependent allergic lung disease (141.1)" @default.
- W2286611921 doi "https://doi.org/10.4049/jimmunol.184.supp.141.1" @default.
- W2286611921 hasPublicationYear "2010" @default.
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