ArticleInflammatory bowel diseases2011
Relationship between inflammation and tissue hypoxia in a mouse model of chronic colitis.
Article in Inflammatory bowel diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 21 citations in OpenAlex.
- HIF-2α-dependent induction of miR-29a restrains TNature communications · 2024Article
- Chronic cigarette smoke exposure induces systemic hypoxia that drives intestinal dysfunction.JCI insight · 2018Article
- Qingchang Suppository Ameliorates Colonic Vascular Permeability in Dextran-Sulfate-Sodium-Induced Colitis.Frontiers in pharmacology · 2018Article
- Immunosuppressive monocytes: possible homeostatic mechanism to restrain chronic intestinal inflammation.Journal of leukocyte biology · 2014Article
- Ocular dysfunction in a mouse model of chronic gut inflammation.Inflammatory bowel diseases · 2013Article
- Relationship among circulating leukocytes, platelets, and microvascular responses during induction of chronic colitis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2011Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHypoxia has been reported to be associated with the colonic inflammation observed in a chemically induced mouse model of self-limiting colitis, suggesting that low tissue oxygen tension may play a role in the pathophysiology of inflammatory tissue injury. However, no studies have been reported evaluating whether tissue hypoxia is associated with chronic gut inflammation. Therefore, the objective of the present study was to determine whether hypoxia is produced within the colon during the development of chronic gut inflammation.
methodsAdoptive transfer of CD4(+) T cells obtained from interleukin-10-deficient (IL-10(-/-)) mice into lymphopenic recombinase-activating gene-1-deficient (RAG(-/-)) mice induces chronic colonic inflammation, with the inflammation ranging from mild to severe as determined by blinded histological analyses. Colonic blood flow, hematocrit, and vascular density were determined using standard protocols, whereas tissue hypoxia was determined using the oxygen-dependent probe pimonidazole.
resultsAdoptive transfer of IL-10(-/-) CD4(+) T cells into RAG(-/-) recipients induced chronic colonic inflammation that ranged from mild to severe at 8 weeks following T-cell transfer. The colitis was characterized by bowel wall thickening, goblet cell dropout, and inflammatory infiltrate. Surprisingly, we found that animals exhibiting mild colonic inflammation had increased hypoxia and decreased systemic hematocrit, whereas mice with severe colitis exhibited levels of hypoxia and hematocrit similar to healthy controls. In addition, we observed that the extent of hypoxia correlated inversely with hematocrit and vascular density.
conclusionsChanges in hematocrit, vascular density, and inflammatory state appear to influence the extent of tissue oxygenation in the T-cell-mediated model of chronic gut inflammation.
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