ArticleEuropean journal of immunology2016
Alterations to chromatin in intestinal macrophages link IL-10 deficiency to inappropriate inflammatory responses.
Article in European journal of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
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- The Role of Tissue-Resident Macrophages in the Development and Treatment of Inflammatory Bowel Disease.Frontiers in cell and developmental biology · 2022Review
- BET Protein Inhibition Regulates Macrophage Chromatin Accessibility and Microbiota-Dependent Colitis.Frontiers in immunology · 2022Article
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- Epigenomic and transcriptomic analysis of chronic inflammatory diseases.Genes & genomics · 2021Review
- The role of inflammatory cytokines in anemia and gastrointestinal mucosal injury induced by foot electric stimulation.Scientific reports · 2021Article
- Gut Microbiota-Mediated Transformation of Coptisine Into a Novel Metabolite 8-Oxocoptisine: Insight Into Its Superior Anti-Colitis Effect.Frontiers in pharmacology · 2021Article
- Distinct Features of Human Myeloid Cell Cytokine Response Profiles Identify Neutrophil Activation by Cytokines as a Prognostic Feature during Tuberculosis and Cancer.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Loss of IL-10 signaling in macrophages limits bacterial killing driven by prostaglandin E2.The Journal of experimental medicine · 2020Article
- Epigenetic regulation of macrophages: from homeostasis maintenance to host defense.Cellular & molecular immunology · 2020Review
- Macrophages in intestinal inflammation and resolution: a potential therapeutic target in IBD.Nature reviews. Gastroenterology & hepatology · 2019Review
- Redefining the IBDs using genome-scale molecular phenotyping.Nature reviews. Gastroenterology & hepatology · 2019Review
- Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies.Nature communications · 2018Article
- Functional macrophages and gastrointestinal disorders.World journal of gastroenterology · 2018Review
- Proinflammatory Role of Monocyte-Derived CX3CR1Infection and immunity · 2018Article
- Origin, Differentiation, and Function of Intestinal Macrophages.Frontiers in immunology · 2018Review
- A distinct epigenetic profile distinguishes stenotic from non-inflamed fibroblasts in the ileal mucosa of Crohn's disease patients.PloS one · 2018Article
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16 authors at 3 institutions in 3 countries.
Funding
Abstract
Intestinal macrophages (IMs) are uniquely programmed to tolerate exposure to bacteria without mounting potent inflammatory responses. The cytokine IL-10 maintains the macrophage anti-inflammatory response such that loss of IL-10 results in chronic intestinal inflammation. To investigate how IL-10-deficiency alters IM programming and bacterial tolerance, we studied changes in chromatin accessibility in response to bacteria in macrophages from two distinct niches, the intestine and bone-marrow, from both wild-type and IL-10-deficient (Il10(-/-) ) mice. We identified chromatin accessibility changes associated with bacterial exposure and IL-10 deficiency in both bone marrow derived macrophages and IMs. Surprisingly, Il10(-/-) IMs adopted chromatin and gene expression patterns characteristic of an inflammatory response, even in the absence of bacteria. Further, when recombinant IL-10 was added to Il10(-/-) cells, it could not revert the chromatin landscape to a normal state. Our results demonstrate that IL-10 deficiency results in stable chromatin alterations in macrophages, even in the absence of bacteria. This supports a model in which IL-10-deficiency leads to chromatin alterations that contribute to a loss of IM tolerance to bacteria, which is a primary initiating event in chronic intestinal inflammation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.