Attachment of a noninvasive enteric pathogen, enteropathogenic Escherichia coli, to cultured human intestinal epithelial monolayers induces transmigration of neutrophils

Enteropathogenic Escherichia coli Interleukin 8 Caco-2 N-Formylmethionine leucyl-phenylalanine Intestinal epithelium
DOI: 10.1128/iai.64.11.4480-4487.1996 Publication Date: 2020-01-06T18:54:09Z
ABSTRACT
An intense inflammatory cell infiltrate, consisting primarily of polymorphonuclear leukocytes (PMN), accompanies enteric infection by enteropathogenic Escherichia coli (EPEC). The mechanism(s) which this pathogen elicits PMN recruitment has not been studied. To determine whether EPEC intestinal epithelial cells induces to transmigrate, an in vitro model cultured human monolayers (T84), a strain (E2348/69), and isolated was used. Results these studies showed that attachment T84 stimulated the transepithelial migration dose-dependent fashion. This event attributable classic bacterial chemoattractants, n-formylated peptides, or other soluble factors. A nonadherent strain, JPN15, unable cause cross monolayer. Epithelial protein synthesis required for maximum EPEC-induced transmigration occur. Transfer assays demonstrated presence chemokine sterilized medium from infected monolayers. Neutralizing antibodies interleukin 8 ablated approximately 50% chemotactic activity. Studies with mutant strains revealed eaeB gene, activation signal transduction pathways host cells, crucial eliciting transmigration. These data show first time noninvasive findings strongly suggest target activates cascade ultimately leads expression release epithelium-derived factor(s) PMN.
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