Journal
PLOS ONE
Volume 8, Issue 10, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0078099
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Funding
- Global COE Program
- Ministry of Education, Culture, Sports, Science and Technology (MEXT)
- Ministry of Health, Labour and Welfare, Japan
- Grant of National Center for Child Health and Development [23A-5]
- Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency
- Grants-in-Aid for Scientific Research [25860805, 25461168, 23390262] Funding Source: KAKEN
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Both interleukin (IL)-33 and IL-25 induce Th2 cytokine production by various cell types, suggesting that they contribute to development of allergic disorders. However, the precise roles of IL-33 and IL-25 in house dust mite (HDM)-induced allergic rhinitis (AR) remain unclear. Both IL-33 and IL-25 were produced mainly by nasal epithelial cells during HDM-induced AR. Eosinophil and goblet cell counts in the nose and IL-5 levels in lymph node cell culture supernatants were significantly decreased in IL-33-deficient, but not IL-25-deficient, mice compared with wild-type mice during HDM-induced AR, but the serum IgE and IgG1 levels did not differ. On the other hand, HDM-induced AR developed similarly in wild-type mice transferred with either IL-33-deficient BM cells or wild-type BM cells. IL-33, but not IL-25, produced by nasal epithelial cells was crucial for the development of murine HDM-induced AR. These observations suggest that IL-33 neutralization may be a potential approach for treatment of HDM-induced AR in humans.
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