ArticleInfection and immunity2014
Host inflammatory response inhibits Escherichia coli O157:H7 adhesion to gut epithelium through augmentation of mucin expression.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- Deoxynivalenol modulated mucin expression and proinflammatory cytokine production, affecting susceptibility to enteroinvasive Escherichia coli infection in intestinal epithelial cells.Journal of food science · 2025Article
- Cannabidiol Enhances Mitochondrial Metabolism and Antioxidant Defenses in Human Intestinal Epithelial Caco-2 Cells.Nutrients · 2024Article
- Differential Colonization and Mucus Ultrastructure Visualization in Bovine Ileal and Rectal Organoid-Derived Monolayers Exposed to EnterohemorrhagicInternational journal of molecular sciences · 2024Article
- Article
- CommensalAnimals : an open access journal from MDPI · 2023Article
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- Role of gut microbiota and bacterial metabolites in mucins of colorectal cancer.Frontiers in cellular and infection microbiology · 2023Review
- EnterotoxigenicFrontiers in immunology · 2022Review
- Effect of Cooking Methods on Bioactivity of Polyphenols in Purple Potatoes.Antioxidants (Basel, Switzerland) · 2021Article
- The glycosyltransferase ST3GAL2 is regulated by miR-615-3p in the intestinal tract of Campylobacter jejuni infected mice.Gut pathogens · 2021Article
- Article
- Transcriptomic Analysis of Shiga Toxin-ProducingMicroorganisms · 2020Article
- The Role ofToxins · 2020Review
- Enteric Immunity: Happy Gut, Healthy Animal.The Veterinary clinics of North America. Food animal practice · 2018Review
- Frontline defenders: goblet cell mediators dictate host-microbe interactions in the intestinal tract during health and disease.American journal of physiology. Gastrointestinal and liver physiology · 2018Review
- Suppressing autophagy: a strategy by Escherichia coli O157:H7 for its survival on host epithelial cells.Cell death & disease · 2018Article
- Overexpression of Toll-like Receptor 4-linked Mitogen-activated Protein Kinase Signaling Contributes to Internalization ofInternational journal of biological sciences · 2018Article
- Functional Enterospheres Derived In Vitro from Human Pluripotent Stem Cells.Stem cell reports · 2017Article
- Complete Genome Sequence ofGenome announcements · 2017Article
- The StcE metalloprotease of enterohaemorrhagic Escherichia coli reduces the inner mucus layer and promotes adherence to human colonic epithelium ex vivo.Cellular microbiology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Escherichia coli O157:H7, a major Shiga toxin-producing pathogen, has a low infectious dose and causes serious illness in humans. The gastrointestinal tract of cattle is the primary reservoir of E. coli O157:H7, and thus, it is critical to eliminate or reduce E. coli O157:H7 gut colonization. Given that E. coli O157:H7 produces effectors that attenuate inflammatory signaling, we hypothesized that the host inflammatory response acts to perturb E. coli O157:H7 intestinal colonization. Tumor necrosis factor alpha (TNF-α) treatment of HT-29 cells resulted in increased expression of inflammatory cytokine interleukin 1β (IL-1β), IL-8, and TNF-α genes and increased IL-8 protein and resulted in decreased adhesion of E. coli O157:H7. Similarly, E. coli O157:H7 adhesion to cattle colonic explants was reduced by TNF-α treatment. Irrespective of the presence of E. coli O157:H7, TNF-α enhanced activation of p65, the key mediator of NF-κB inflammatory signaling, whereas E. coli O157:H7 infection suppressed this pathway by inhibiting p65 activation in HT-29 cells. To further explore the mechanisms linking the inflammatory response to attenuated E. coli O157:H7 adhesion, mucin 2 (MUC2) expression was analyzed, considering that the intestinal mucus layer is the first defense against enteric pathogens and MUC2 is the major secretory mucin in the intestine. MUC2 expression in HT-29 cells was increased by TNF-α treatment and by E. coli O157:H7 infection. However, reducing mucin expression by blocking mitogen-activated protein kinase (MAPK) extracellular signal-regulated protein kinases 1/2 (ERK1/2) and/or phosphatidylinositol 3-kinase (PI3K)/Akt signaling increased E. coli O157:H7 adherence to HT-29 cells. These data suggest that the inflammatory cytokine response acts to protect host epithelial cells against E. coli O157:H7 colonization, at least in part, by promoting mucin production.
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