Long polar fimbriae participates in the induction of neutrophils transepithelial migration across intestinal cells infected with enterohemorrhagic E. coli O157:H7
Author
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Vergara, Alejandra F.
Author
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Vidal, Roberto M.
Author
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Torres, Alfredo G.
Author
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Farfán Urzúa, Mauricio
Admission date
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2015-07-15T13:35:45Z
Available date
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2015-07-15T13:35:45Z
Publication date
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2015
Cita de ítem
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Frontiers in Cellular and Infection Microbiology January 2015 | Volume 4 | Article 185
en_US
Identifier
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DOI: 10.3389/fcimb.2014.00185
Identifier
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https://repositorio.uchile.cl/handle/2250/131978
General note
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Artículo de publicación ISI
en_US
Abstract
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Enterohemorrhagic Escherichia coli (EHEC) strains are causative agents of diarrhea and hemorrhagic colitis, both diseases associated with intestinal inflammation and cell damage. Several studies have correlated EHEC virulence factors to high levels of intestinal pro-inflammatory cytokines and we have previously described that the Long polar fimbriae (Lpf) is involved in the secretion of interleukin-8 (IL-8) and up-regulation of genes belonging to the NE-kappa B pathway using non-polarized epithelial intestinal 184 cells. In the current study, we evaluated the two EHEC 0157 Lpf fimbriae (Lpf1 and Lpf2) for their ability to induce intestinal secretion of IL-8 and the activation of IL8, CCL20, and ICAM1 genes on polarized 184 cells. We also determined the participation of Lpf1 and Lpf2 in transepithelial migration of polymorphonuclear neutrophils (PMNs). Polarized 184 cells infected with EHEC revealed that both, Lpf1 and Lpf2, were required for the secretion of IL-8 and the induction of IL8, CCL20, and ICAM1 genes. Both fimbriae also played a role in the migration of PMNs trough the intestinal cells monolayer. Overall, the present work further demonstrated that the fimbriae Lpf1 and Lpf2 are important bacterial virulence factors that might be involved in the inflammatory responses associated with EHEC infections.
Long polar fimbriae participates in the induction of neutrophils transepithelial migration across intestinal cells infected with enterohemorrhagic E. coli O157:H7