IL-1 beta in eosinophil-mediated small intestinal homeostasis and IgA production
- Authors
- Jung, Y.; Wen, T.; Mingler, M. K.; Caldwell, J. M.; Wang, Y. H.; Chaplin, D. D.; Lee, E. H.; Jang, M. H.; Woo, S. Y.; Seoh, J. Y.; Miyasaka, M.; Rothenberg, M. E.
- Issue Date
- Jul-2015
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- MUCOSAL IMMUNOLOGY, v.8, no.4, pp.930 - 942
- Journal Title
- MUCOSAL IMMUNOLOGY
- Volume
- 8
- Number
- 4
- Start Page
- 930
- End Page
- 942
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/10387
- DOI
- 10.1038/mi.2014.123
- ISSN
- 1933-0219
- Abstract
- Eosinophils are multifunctional leukocytes that reside in the gastrointestinal (GI) lamina propria, where their basal function remains largely unexplored. In this study, by examining mice with a selective deficiency of systemic eosinophils (by lineage ablation) or GI eosinophils (eotaxin-1/2 double deficient orCC chemokine receptor 3 deficient), we show that eosinophils support immunoglobulin A (IgA) class switching, maintain intestinal mucus secretions, affect intestinal microbial composition, and promote the development of Peyer's patches. Eosinophil-deficient mice showed reduced expression of mediators of secretory IgA production, including intestinal interleukin 1 beta (IL-1 beta), inducible nitric oxide synthase, lymphotoxin (LT) alpha, and LT-beta, and reduced levels of retinoic acid-related orphan receptor gamma t-positive (ROR-gamma t(+)) innate lymphoid cells (ILCs), while maintaining normal levels of APRIL (a proliferation-inducing ligand), BAFF (B cell-activating factor of the tumor necrosis factor family), and TGF-beta (transforming growth factor beta). GI eosinophils expressed a relatively high level of IL-1 beta, and IL-1 beta-deficient mice manifested the altered gene expression profiles observed in eosinophil-deficient mice and decreased levels of IgA(+) cells and ROR-gamma t(+) ILCs. On the basis of these collective data, we propose that eosinophils are required for homeostatic intestinal immune responses including IgA production and that their affect is mediated via IL-1 beta in the small intestine.
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