| Commensal microbiota induce LPS hyporesponsiveness in colonic macrophages via the production of IL-10. | |
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MedLine Citation:
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PMID: 21051439 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Several subsets of innate immune cells, all with unique properties, reside within the intestinal lamina propria. However, compared with intestinal dendritic cells (DCs), intestinal macrophages are less well characterized. In this study, we examined the properties of macrophages in the colonic lamina propria (LM). Colonic DCs (LDC) showed LPS-induced production of IL-12p40. In contrast, LM showed constitutive IL-10 production and unresponsiveness to LPS in terms of inflammatory cytokine production. Comparison of the gene expression profiles between LM and LDC revealed that LM preferentially expressed IL-10-related genes. LM obtained from mice lacking IL-10 or Stat3 showed hyperproduction of tumour necrosis factor (TNF)-α and IL-6 in response to LPS. IL-10 production in the large intestine was mainly induced by LM and regulatory T cells and was dependent on the presence of commensal microbiota. Accordingly, LM from germ-free mice showed less production of IL-10 and increased levels of LPS-induced TNF-α and IL-6 production. Taken together, these results demonstrate that the activity of LM to produce pro-inflammatory cytokines is negatively regulated through commensal microbiota-dependent IL-10 production in the large intestine. |
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Authors:
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Yoshiyasu Ueda; Hisako Kayama; Seong Gyu Jeon; Takashi Kusu; Yoshitaka Isaka; Hiromi Rakugi; Masahiro Yamamoto; Kiyoshi Takeda |
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Publication Detail:
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Type: Journal Article Date: 2010-11-03 |
Journal Detail:
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Title: International immunology Volume: 22 ISSN: 1460-2377 ISO Abbreviation: Int. Immunol. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-12-14 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8916182 Medline TA: Int Immunol Country: England |
Other Details:
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Languages: eng Pagination: 953-62 Citation Subset: IM |
Affiliation:
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Laboratory of Immune Regulation, Department of Microbiology and Immunology, Graduate School of Medicine. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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