INTRACELLULAR PERSISTENCE OF ENTEROAGGREGATIVE ESCHERICHIA COLI INDUCES A PROINFLAMMATORY CYTOKINES SECRETION IN INTESTINAL EPITHELIAL T84 CELLS

The competence of enteroaggregative Escherichia coli (EAEC) to adhere to the intestinal epithelium of the host is a key role to the colonization and disease development. The virulence genes are crucial for EAEC pathogenicity during adherence, internalization and persistence in the host. The overwhel...

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Veröffentlicht in:Arquivos de gastroenterologia 2018-04, Vol.55 (2), p.133-137
Hauptverfasser: Braga, Ricardo Luís Lopes, Pereira, Ana Claudia Machado, Ferreira, Andréa Fonseca, Rosa, Ana Cláudia de Paula, Pereira-Manfro, Wânia Ferraz
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Sprache:eng
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Zusammenfassung:The competence of enteroaggregative Escherichia coli (EAEC) to adhere to the intestinal epithelium of the host is a key role to the colonization and disease development. The virulence genes are crucial for EAEC pathogenicity during adherence, internalization and persistence in the host. The overwhelming majority of antigen encounters in a host occurs on the intestine surface, which is considered a part of innate mucosal immunity. Intestinal epithelial cells (IECs) can be activated by microorganisms and induce an immune response. The present study investigated the interaction of invasive EAEC strains with T84 intestinal epithelial cell line in respect to bacterial invasiveness, persistence and cytokines production. We evaluated intracellular persistence of invasive EAEC strains (H92/3, I49/3 and the prototype 042) and production of cytokines by sandwich ELISA in T84 cells upon 24 hours of infection. The survival rates of the prototype 042 was 0.5x103 CFU/mL while survival of I49/3 and H92/3 reached 3.2x103 CFU/mL and 1.4x103 CFU/mL, respectively. Infection with all EAEC strains tested induced significant amounts of IL-8, IL-6 and TNF-α compared to uninfected T84 cells. These data showed that infection by invasive EAEC induce a proinflammatory immune response in intestinal epithelial T84 cells.
ISSN:0004-2803
1678-4219
1678-4219
DOI:10.1590/S0004-2803.201800000-23