Immunobiology 223 (2018) 38–48 Contents lists available at ScienceDirect Immunobiology journal homepage: www.elsevier.com/locate/imbio TLR2 activation induced by H. pylori LPS promotes the diﬀerential MARK expression of claudin-4, -6, -7 and -9 via either STAT3 and ERK1/2 in AGS cells Christian O. Chavarría-Velázquez, Ana C. Torres-Martínez, Luis F. Montaño, Erika P. Rendón-Huerta Laboratorio de Inmunobiología, Depto. Biología Celular y Tisular, Facultad de Medicina, UNAM, Mexico ARTICLE I NFO ABSTRACT Keywords: Gastric carcinogenesis has been associated to H. pylori virulence factors that induce a chronic inﬂammation Helicobacter pylori process. Lipopolysaccharides play a role in chronic inﬂammatory responses via TLR2- and TLR4-dependent Toll-like receptors signaling pathways. Similarly, cellular invasiveness, metastatic potential and prognosis are usually associated to Lipopolysaccharide claudin-4, -6, -7 and -9 expression in gastric carcinogenesis. Therefore, the aim of this study was to determine if Claudins H. pylori LPS exerts an inﬂuence on carcinogenesis-related claudin expression and if it was directly regulated ERK1/2 through the TLR2 pathway. Human antrum gastric adenocarcinoma AGS cells exposed or not to H. pylori LPS STAT3 were used. Polyclonal anti-claudin-4, -6, -7 and -9, anti-TLR2, anti-pERK1/2 as well as rabbit monoclonal anti- pNFκB p65 and mouse monoclonal anti-CdX2 were used. ERK1/2 inhibitor UO126 and STAT3
Immunobiology – Elsevier
Published: Jan 1, 2018
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