ArticleMucosal immunology2012
Colonic epithelial response to injury requires Myd88 signaling in myeloid cells.
Article in Mucosal immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 46 citations in OpenAlex.
- What we know about prostaglandin pathway dysfunction in chronic enteropathies: From endoscopy to molecular diagnosis.Journal of translational internal medicine · 2026Article
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- Monocyte-macrophages modulate intestinal homeostasis in inflammatory bowel disease.Biomarker research · 2024Review
- MyD88 in macrophages protects against colitis via inhibiting the activation of NLRP3 inflammasome in epithelial cells.Genes & diseases · 2023Article
- Macrophage orchestration of epithelial and stromal cell homeostasis in the intestine.Journal of leukocyte biology · 2022Review
- Regulatory role of short-chain fatty acids in inflammatory bowel disease.Cell communication and signaling : CCS · 2022Review
- Impact of Microbial Metabolites on Microbiota-Gut-Brain Axis in Inflammatory Bowel Disease.International journal of molecular sciences · 2021Review
- Acute Intestinal Inflammation Depletes/Recruits Histamine-Expressing Myeloid Cells From the Bone Marrow Leading to Exhaustion of MB-HSCs.Cellular and molecular gastroenterology and hepatology · 2021Article
- Intestinal resident macrophages: Multitaskers of the gut.Neurogastroenterology and motility · 2020Review
- Hyaluronic acid promotes Lgr5American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Caveolar communication with xenobiotic-stalled ribosomes compromises gut barrier integrity.Communications biology · 2020Article
- Nonmicrobial Activation of TLRs Controls Intestinal Growth, Wound Repair, and Radioprotection.Frontiers in immunology · 2020Review
- Tryptophan Metabolites Along the Microbiota-Gut-Brain Axis: An Interkingdom Communication System Influencing the Gut in Health and Disease.International journal of tryptophan research : IJTR · 2020Review
- Glutamatergic Signaling Along The Microbiota-Gut-Brain Axis.International journal of molecular sciences · 2019Review
- Resident Immunity in Tissue Repair and Maintenance: The Zebrafish Model Coming of Age.Frontiers in cell and developmental biology · 2019Article
- Review
- Immunity to gastrointestinal nematode infections.Mucosal immunology · 2018Review
- Leukocyte-Derived Interleukin-10 Aggravates Postoperative Ileus.Frontiers in immunology · 2018Article
- Barrier-tissue macrophages: functional adaptation to environmental challenges.Nature medicine · 2017Review
- Gut microbiota and IBD: causation or correlation?Nature reviews. Gastroenterology & hepatology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Proper colonic injury response requires myeloid-derived cells and Toll-like receptor/Myd88 signaling. However, the precise role of Myd88 signaling specifically in myeloid-derived cells that occurs during tissue damage is unclear. Therefore, we created a mouse line with Myd88 expression restricted to myeloid lineages (Myd88(-/-); LysM(Cre/+); ROSA26(Myd88/+); herein Mlcr). In these mice, Myd88 was appropriately expressed and mediated responses to bacterial ligand exposure in targeted cells. Importantly, the severe colonic epithelial phenotype observed in dextran sodium sulfate-injured Myd88(-/-) mice was rescued by the genetic modification of Mlcr mice. During injury, myeloid cell activation and enrichment of Ptsg2-expressing stromal cells occurred within the mesenchyme that surrounded the crypt bases of Mlcr and Myd88(+/-) mice but not Myd88(-/-) mice. Interestingly, these cellular changes to the crypt base mesenchyme also occurred, but to a lesser extent in uninjured Mlcr mice. These results show that Myd88 expression in myeloid cells was sufficient to rescue intestinal injury responses, and surprisingly, these cells appear to require an additional Myd88-dependent signal from a non-myeloid cell type during homeostasis.
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What OpenQuestion holds
Registered trials
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.