FEBS letters · 2001
Production of beta-defensin-2 by human colonic epithelial cells induced by Salmonella enteritidis flagella filament structural protein.
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Takahashi A, Wada A, Ogushi K, Maeda K, Kawahara T, Mawatari K, Kurazono H, Moss J, Hirayama T, Nakaya Y
Аннотация
We recently showed that FliC of Salmonella enteritidis increased human beta-defensin-2 (hBD-2) expression, and now describe the signaling responsible pathway. FliC increased the intracellular Ca(2+) concentration ([Ca(2+)](in)) in Caco-2 cells. The [Ca(2+)](in) increase induced by FliC was prevented by U73122 and heparin, but not by chelating extracellular Ca(2+) or pertussis toxin. The FliC-induced increase in hBD-2 promoter activity via nuclear factor kappaB (NF-kappaB) was also inhibited by chelation of intracellular Ca(2+) or by U73122. We conclude that FliC increased [Ca(2+)](in) via inositol 1,4,5-trisphosphate, which was followed by up-regulating hBD-2 mRNA expression via an NF-kappaB-dependent pathway.
Предметные рубрики MeSH
Caco-2 CellsCalciumCell NucleusChelating AgentsColonCulture MediaEgtazic AcidEstrenesFlagellinHeparinHumansInositol 1,4,5-TrisphosphateIntestinal MucosaNF-kappa BPertussis ToxinPromoter Regions, GeneticPyrrolidinonesRNA, MessengerSalmonella enteritidisSignal TransductionUp-RegulationVirulence Factors, Bordetellabeta-Defensins