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- W28981503 abstract "Objectives Pulmonary edema, which involves a reduced alveolar Na+ uptake capacity, can be a major complication of listeriosis. We have investigated the effect of the main virulence factor of L. monocytogenes, i.e. listeriolysin (LLO), on the expression of the crucial alpha subunit of ENaC and on Protein Kinase C (PKC)-alpha, a negative regulator of ENaC expression, in the human H441 cell line. We moreover assessed LLO effects on amiloride-sensitive Na+ currents in vitro and on edema formation in vivo. Results ENaC-alpha expression and amiloride-sensitive sodium uptake in H441 cells are significantly decreased upon LLO-treatment, an effect completely blunted by the PKC-alpha inhibitor Ro-32-0432. The TNF-derived TIP peptide blocks LLO-mediated PKC-alpha activation, significantly restores ENaC-alpha expression and increases amiloride-sensitive Na+ uptake. In vivo, LLO, upon intratracheal instillation, significantly increases lung wet-to-dry ratio, which can be blunted by the TIP peptide. Conclusion These results demonstrate that LLO contributes to edema formation by reducing ENaC function in a PKC-alpha-dependent manner. The TIP peptide restores impaired ENaC expression and activates Na+ uptake in LLO-treated airway epithelial cells, thus indicating its therapeutic potential for the treatment of listeriosis-related permeability edema. (Supported by grant RO1HL094609 from the NHBLI)" @default.
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- W28981503 date "2011-04-01" @default.
- W28981503 modified "2023-10-16" @default.
- W28981503 title "Role of Protein Kinase C‐alpha in Listeriolysin‐induced ENaC dysfunction in human airway epithelial cells" @default.
- W28981503 doi "https://doi.org/10.1096/fasebj.25.1_supplement.1039.22" @default.
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