| Literature DB >> 22331917 |
Koubun Yasuda1, Taichiro Muto, Tatsukata Kawagoe, Makoto Matsumoto, Yuki Sasaki, Kazufumi Matsushita, Yuko Taki, Shizue Futatsugi-Yumikura, Hiroko Tsutsui, Ken J Ishii, Tomohiro Yoshimoto, Shizuo Akira, Kenji Nakanishi.
Abstract
When animals are infected with helminthic parasites, resistant hosts show type II helper T immune responses to expel worms. Recently, natural helper (NH) cells or nuocytes, newly identified type II innate lymphoid cells, are shown to express ST2 (IL-33 receptor) and produce IL-5 and IL-13 when stimulated with IL-33. Here we show the relevant roles of endogenous IL-33 for Strongyloides venezuelensis infection-induced lung eosinophilic inflammation by using Il33(-/-) mice. Alveolar epithelial type II cells (ATII) express IL-33 in their nucleus. Infection with S. venezuelensis or intranasal administration of chitin increases in the number of ATII cells and the level of IL-33. S. venezuelensis infection induces pulmonary accumulation of NH cells, which, after being stimulated with IL-33, proliferate and produce IL-5 and IL-13. Furthermore, S. venezuelensis infected Rag2(-/-) mice increase the number of ATII cells, NH cells, and eosinophils and the expression of IL-33 in their lungs. Finally, IL-33-stimulated NH cells induce lung eosinophilic inflammation and might aid to expel infected worms in the lungs.Entities:
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Year: 2012 PMID: 22331917 PMCID: PMC3295287 DOI: 10.1073/pnas.1201042109
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205