ArticleInfection and immunity2009
Decreased expression of colonic Slc26a3 and carbonic anhydrase iv as a cause of fatal infectious diarrhea in mice.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 81 citations in OpenAlex.
- Akkermansia muciniphila isolated from forest musk deer ameliorates diarrhea in mice via modification of gut microbiota.Animal models and experimental medicine · 2025Article
- Assessing Native Liver Post-Kasai Portoenterostomy for Biliary Atresia Through Stool Proteome Analysis.Gastro hep advances · 2025Article
- Ulcerative colitis: molecular insights and intervention therapy.Molecular biomedicine · 2024Review
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- Epithelial dysfunction is prevented by IL-22 treatment in a Citrobacter rodentium-induced colitis model that shares similarities with inflammatory bowel disease.Mucosal immunology · 2022Article
- Transcriptional Profiling of the Small Intestine and the Colon Reveals Modulation of Gut Infection withNutrients · 2022Article
- A nonredundant role for T cell-derived interleukin 22 in antibacterial defense of colonic crypts.Immunity · 2022Article
- Article
- A Novel Role of SLC26A3 in the Maintenance of Intestinal Epithelial Barrier Integrity.Gastroenterology · 2021Article
- Segmental differences in Slc26a3-dependent ClThe journal of physiological sciences : JPS · 2021Article
- Epithelial transport in digestive diseases: mice, monolayers, and mechanisms.American journal of physiology. Cell physiology · 2020Review
- Decreased SLC26A3 expression and function in intestinal epithelial cells in response toAmerican journal of physiology. Cell physiology · 2019Article
- Uncoupling of Carbonic Anhydrase from Na-H exchanger-1 in Experimental Colitis: A Possible Mechanistic Link with Na-H Exchanger.Biomolecules · 2019Article
- Citrobacter rodentium-host-microbiota interactions: immunity, bioenergetics and metabolism.Nature reviews. Microbiology · 2019Review
- Association of ulcerative colitis with solute-linked carrier family 26 member A3 gene polymorphisms and its expression in colonic tissues in Chinese patients.International journal of colorectal disease · 2018Article
- Infection with enteric pathogens Salmonella typhimurium and Citrobacter rodentium modulate TGF-beta/Smad signaling pathways in the intestine.Gut microbes · 2018Article
- Human evolutionary loss of epithelial Neu5Gc expression and species-specific susceptibility to cholera.PLoS pathogens · 2018Article
- miR-130a and miR-212 Disrupt the Intestinal Epithelial Barrier through Modulation of PPARγ and Occludin Expression in Chronic Simian Immunodeficiency Virus-Infected Rhesus Macaques.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Loss of disease tolerance during Citrobacter rodentium infection is associated with impaired epithelial differentiation and hyperactivation of T cell responses.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Citrobacter rodentium causes epithelial hyperplasia and colitis and is used as a model for enteropathogenic and enterohemorrhagic Escherichia coli infections. Little or no mortality develops in most inbred strains of mice, but C3H and FVB/N mice exhibit fatal outcomes of infection. Here we test the hypothesis that decreased intestinal transport activity during C. rodentium infection results in fatality in C3H/HeOu and FVB/N mice. Susceptible strains were compared to resistant C57BL/6 mice and to inbred strains SWR and SJL of Swiss origin, which have not been previously characterized for outcomes of C. rodentium infection. Mortality in susceptible strains C3H/HeOu and FVB/N was associated with significant fluid loss in feces, a remarkable downregulation of Slc26a3 and carbonic anhydrase IV (CAIV) message and protein expression, retention of chloride in stool, and hypochloremia, suggesting defects in intestinal chloride absorption. SWR, SJL, and C57BL/6 mice were resistant and survived the infection. Fluid therapy fully prevented mortality in C3H/HeOu and FVB/N mice without affecting clinical disease. Common pathogenic mechanisms, such as decreased levels of expression of Slc26a3 and CAIV, affect intestinal ion transport in C. rodentium-infected FVB and C3H mice, resulting in profound electrolyte loss, dehydration, and mortality. Intestinal chloride absorption pathways are likely a potential target for the treatment of infectious diarrhea.
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