ArticlePloS one2011
Bacterial-epithelial contact is a key determinant of host innate immune responses to enteropathogenic and enteroaggregative Escherichia coli.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 49 citations in OpenAlex.
- EnteropathogeniceLife · 2026Article
- Metabolites of non-aureus staphylococci affect the ability of Staphylococcus aureus to adhere to and internalize into bovine mammary epithelial cells.Veterinary research · 2023Article
- Pathophysiology of enteropathogenicJournal of veterinary science · 2022Review
- Identification of mucin degraders of the human gut microbiota.Scientific reports · 2021Article
- Faecal cytokine profiling as a marker of intestinal inflammation in acutely decompensated cirrhosis.JHEP reports : innovation in hepatology · 2020Article
- Microbial adaptation to the healthy and inflamed gut environments.Gut microbes · 2020Review
- Identification and characterisation of enteroaggregative Escherichia coli subtypes associated with human disease.Scientific reports · 2020Article
- Worm-Based Alternate Assessment of Probiotic Intervention against Gut Barrier Infection.Nutrients · 2019Article
- Pet serine protease from enteroaggregative Escherichia coli stimulates the inflammatory response activating human macrophages.BMC microbiology · 2016Article
- Pancreatic amylase is an environmental signal for regulation of biofilm formation and host interaction in Campylobacter jejuni.Infection and immunity · 2015Article
- Serratia marcescens is injurious to intestinal epithelial cells.Gut microbes · 2014Article
- The impact of simvastatin on pulmonary effectors of Pseudomonas aeruginosa infection.PloS one · 2014Article
- Article
- Recent advances in understanding enteric pathogenic Escherichia coli.Clinical microbiology reviews · 2013Review
- Pathogenesis of human enterovirulent bacteria: lessons from cultured, fully differentiated human colon cancer cell lines.Microbiology and molecular biology reviews : MMBR · 2013Review
- Prolonged NF-κB activation by a macrophage inhibitory cytokine 1-linked signal in enteropathogenic Escherichia coli-infected epithelial cells.Infection and immunity · 2013Article
- The role of peroxisome proliferator-activated receptor γ in immune responses to enteroaggregative Escherichia coli infection.PloS one · 2013Article
- Clinical implications of enteroadherent Escherichia coli.Current gastroenterology reports · 2012Review
- Spatial analysis of gut microbiome reveals a distinct ecological niche associated with the mucus layer.Gut microbesArticle
- Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEnteropathogenic (EPEC) and Enteroaggregative (EAEC) E. coli have similar, but distinct clinical symptoms and modes of pathogenesis. Nevertheless when they infect the gastrointestinal tract, it is thought that their flagellin causes IL-8 release leading to neutrophil recruitment and gastroenteritis. However, this may not be the whole story as the effect of bacterial adherence to IEC innate response(s) remains unclear. Therefore, we have characterized which bacterial motifs contribute to the innate epithelial response to EPEC and EAEC, using a range of EPEC and EAEC isogenic mutant strains. METHODOLOGY: Caco-2 and HEp-2 cell lines were exposed to prototypical EPEC strain E2348/69 or EAEC strain O42, in addition to a range of isogenic mutant strains. E69 [LPS, non-motile, non-adherent, type three secretion system (TTSS) negative, signalling negative] or O42 [non-motile, non-adherent]. IL-8 and CCL20 protein secretion was measured. Bacterial surface structures were assessed by negative staining Transmission Electron Microscopy. The Fluorescent-actin staining test was carried out to determine bacterial adherence.
resultsPrevious studies have reported a balance between the host pro-inflammatory response and microbial suppression of this response. In our system an overall balance towards the host pro-inflammatory response is seen with the E69 WT and to a greater extent O42 WT, which is in fit with clinical symptoms. On removal of the external EPEC structures flagella, LPS, BFP, EspA and EspC; and EAEC flagella and AAF, the host inflammatory response is reduced. However, removal of E69 lymphostatin increases the host inflammatory response suggesting involvement in the bacterial mediated anti-inflammatory response.
conclusionEpithelial responses were due to combinations of bacterial agonists, with host-bacterial contact a key determinant of these innate responses. Host epithelial recognition was offset by the microbe's ability to down-regulate the inflammatory response. Understanding the complexity of this host-microbial balance will contribute to improved vaccine design for infectious gastroenteritis.
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