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Am J Physiol Lung Cell Mol Physiol 282: L207-L214, 2002; doi:10.1152/ajplung.00156.2001
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Vol. 282, Issue 2, L207-L214, February 2002

Mediator generation and signaling events in alveolar epithelial cells attacked by S. aureus alpha -toxin

Frank Rose, Gabriele Dahlem, Bernd Guthmann, Friedrich Grimminger, Ulrich Maus, Jörg Hänze, Nils Duemmer, Ulrich Grandel, Werner Seeger, and Hossein Ardeschir Ghofrani

Department of Internal Medicine, Justus-Liebig University, Giessen D-35392, Germany

Staphylococcus aureus alpha -toxin is a pore-forming bacterial exotoxin that has been implicated as a significant virulence factor in human staphylococcal diseases. In primary cultures of rat pneumocyte type II cells and the human A549 alveolar epithelial cell line, purified alpha -toxin provoked rapid-onset phosphatidylinositol (PtdIns) hydrolysis as well as liberation of nitric oxide and the prostanoids PGE2, PGI2, and thromboxane A2. In addition, sustained upregulation of proinflammatory interleukin (IL)-8 mRNA expression and protein secretion occurred. "Priming" with low-dose IL-1beta markedly enhanced the IL-8 response to alpha -toxin, which was then accompanied by IL-6 appearance. The cytokine response was blocked by the intracellular Ca2+-chelating reagent 1,2-bis(2-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid, the protein kinase C inhibitor bis-indolyl maleimide I, as well as two independent inhibitors of nuclear factor-kappa B activation, pyrrolidine dithiocarbamate and caffeic acid phenethyl ester. We conclude that alveolar epithelial cells are highly reactive target cells of staphylococcal alpha -toxin. alpha -Toxin pore-associated transmembrane Ca2+ flux and PtdIns hydrolysis-related signaling with downstream activation of protein kinase C and nuclear translocation of nuclear factor-kappa B are suggested to represent important underlying mechanisms. Such reactivity of the alveolar epithelial cells may be relevant for pathogenic sequelae in staphylococcal lung disease.

Staphylococcus aureus; sepsis; inflammation


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