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• W767679042 abstract "Innate immune responses are regulated in the intestine to prevent excessive inflammation. Here we show that a subset of mouse colonic macrophages constitutively produce the anti-inflammatory cytokine IL-10. In mice infected with Citrobacter rodentium, a model for enteropathogenic Escherichia coli infection in humans, these macrophages are required to prevent intestinal pathology. IL-23 is significantly increased in infected mice with a myeloid cell-specific deletion of IL-10, and the addition of IL-10 reduces IL-23 production by intestinal macrophages. Furthermore, blockade of IL-23 leads to reduced mortality in the context of macrophage IL-10 deficiency. Transcriptome and other analyses indicate that IL-10-expressing macrophages receive an autocrine IL-10 signal. Interestingly, only transfer of the IL-10 positive macrophages could rescue IL-10-deficient infected mice. Therefore, these data indicate a pivotal role for intestinal macrophages that constitutively produce IL-10, in controlling excessive innate immune activation and preventing tissue damage after an acute bacterial infection. Innate immune responses are regulated in the intestine to prevent excessive inflammation. Here the authors demonstrate a pivotal role for intestinal macrophages that constitutively produce IL-10 in controlling excessive innate immune activation and preventing tissue damage after an acute bacterial infection." @default.
• W767679042 created "2016-06-24" @default.
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• W767679042 date "2015-05-11" @default.
• W767679042 modified "2023-10-16" @default.
• W767679042 title "IL-10-producing intestinal macrophages prevent excessive antibacterial innate immunity by limiting IL-23 synthesis" @default.
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• W767679042 doi "https://doi.org/10.1038/ncomms8055" @default.
• W767679042 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4428691" @default.
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• W767679042 hasPublicationYear "2015" @default.
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