ArticleCommunications biology2022
IL-1-dependent enteric gliosis guides intestinal inflammation and dysmotility and modulates macrophage function.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 50 citations in OpenAlex.
- A biomechanical model of inflammation-driven colon hypertrophy and dysmotility: Application to Gulf War Illness.Journal of the mechanical behavior of biomedical materials · 2026Article
- Curcumin AttenuatesAnimals : an open access journal from MDPI · 2026Article
- Intestinal muscularis in health and disease.Communications biology · 2026Review
- Short-chain fatty acids mitigate inflammation and associated metabolic programming of human stem cell-derived enteric glial cells.Journal of neuroinflammation · 2026Article
- Macrophage-glia interactions regulate immune damage to enteric neurons during West Nile virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Enteric nervous system and inflammatory bowel disease.Gastroenterology report · 2026Review
- Microbiota-immune-enteric nervous system interactions in functional constipation: a narrative review and hypothesis-generating framework.Frontiers in immunology · 2026Review
- Glial Connexin-43 Is a Pathogenic Mechanism Promoting Gut Inflammation in Postoperative Ileus Induced by Gut Surgical Manipulation With Potential Relevance to Humans.Cellular and molecular gastroenterology and hepatology · 2026Article
- Article
- Immunization With Bovine Milk Casein Results in Enteric Nervous System Pathology in a Mouse Model of Neuroinflammation.Neurogastroenterology and motility · 2025Article
- Stool Glial Fibrillary Acidic Protein Is Elevated in Progressive Multiple Sclerosis.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- A Maternal and Postnatal Ad Libitum Propionic Acid-Rich Diet in Mice Alters Intestinal Glia Proliferation and Inflammatory Response: Contrary to Effect in the Brain.International journal of molecular sciences · 2025Article
- Use of Human In Vitro Gut Specimens for Translational Neurogastroenterology and Motility in the 21st Century.Neurogastroenterology and motility · 2025Review
- The role of reactive enteric glia-macrophage interactions in acute and chronic inflammation.Neurogastroenterology and motility · 2025Review
- The role of the enteric nervous system in the pathogenesis of Clostridioides difficile infection.Nature reviews. Gastroenterology & hepatology · 2025Review
- Gpr37 modulates the severity of inflammation-induced GI dysmotility by regulating enteric reactive gliosis.iScience · 2025Article
- Intestinal neuron-associated macrophages in health and disease.Nature immunology · 2025Review
- Layer-specific molecular signatures of colon anastomotic healing and leakage in mice.Molecular medicine (Cambridge, Mass.) · 2025Article
- The Physiology of Enteric Glia.Annual review of physiology · 2025Review
- WKB ameliorates DSS-induced colitis through inhibiting enteric glial cells activation and altering the intestinal microbiota.Journal of translational medicine · 2025Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Muscularis Externa Macrophages (ME-Macs) and enteric glial cells (EGCs) are closely associated cell types in the bowel wall, and important interactions are thought to occur between them during intestinal inflammation. They are involved in developing postoperative ileus (POI), an acute, surgery-induced inflammatory disorder triggered by IL-1 receptor type I (IL1R1)-signaling. In this study, we demonstrate that IL1R1-signaling in murine and human EGCs induces a reactive state, named enteric gliosis, characterized by a strong induction of distinct chemokines, cytokines, and the colony-stimulating factors 1 and 3. Ribosomal tagging revealed enteric gliosis as an early part of POI pathogenesis, and mice with an EGC-restricted IL1R1-deficiency failed to develop postoperative enteric gliosis, showed diminished immune cell infiltration, and were protected from POI. Furthermore, the IL1R1-deficiency in EGCs altered the surgery-induced glial activation state and reduced phagocytosis in macrophages, as well as their migration and accumulation around enteric ganglia. In patients, bowel surgery also induced IL-1-signaling, key molecules of enteric gliosis, and macrophage activation. Together, our data show that IL1R1-signaling triggers enteric gliosis, which results in ME-Mac activation and the development of POI. Intervention in this pathway might be a useful prophylactic strategy in preventing such motility disorders and gut inflammation.
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