FEBS Letters · 2001 · 64 citations · 22 references
Life SciencesMicrobiologyMolecular BiologyCell SignalingGene ExpressionSignal TransductionBacterial Gene RegulationBacterial PathogenesisCalcium SignalingInnate Immune Signaling PathwaysIntracellular Calcium SignalingToxin-mediated PathogenesisCa2+ SignalingCalcium-dependent Gene ExpressionCalcium-mediated SignalingDefensin ExpressionNf-kappa B-dependent TranscriptionNuclear Factor Kappa B ActivationNuclear Factor Kappa B InhibitionNuclear Factor Kappa B Modulation
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.
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The innate immune response to bacterial flagellin is mediated by Toll-like receptor 5
Fumitaka Hayashi, Kelly D. Smith, Adrian Ozinsky et al. · Nature · 2001 · 3.6K citations