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Pseudomonas aeruginosa activates Cl channels in host epithelial cells

  • Cell and Molecular Physiology
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Abstract

Exposure to Pseudomonas aeruginosa triggers the apoptotic cell death of Chang epithelial cells, and this depends on the expression of both the CD95 receptor and CD95 ligand. In lymphocytes CD95-mediated apoptosis is paralleled by the activation of outwardly rectifying Cl channels. The present study was performed to explore whether P. aeruginosa-induced apoptosis of Chang epithelial cells is paralleled by activation of Cl channels. According to whole-cell patch-clamp recordings, exposure of Chang epithelial cells to P. aeruginosa does lead to rapid activation of an outwardly rectifying Cl-selective current. The current is inhibited by the Cl channel blocker NPPB. Exposure of Chang epithelial cells to P. aeruginosa led to a significant decrease of cell membrane capacitance by 6%, pointing to a decrease in cell volume by 7%. Exposure to P. aeruginosa depolarized the mitochondrial membrane potential indicating apoptotic cell death. The decline of mitochondrial membrane potential was not significantly affected by NPPB. In conclusion, P. aeruginosa-induced apoptosis of Chang epithelial cells is paralleled by activation of Cl channels. Activation of the channels participates in the alteration of cell volume but is not a prerequisite for P. aeruginosa-induced apoptosis.

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Acknowledgements

The authors gratefully acknowledge the technical assistance of E. Faber. This work was supported by the Deutsche Forschungsgemeinschaft (La 315/4–4), a grant of the Bundesministerium für Bildung, Wissenschaft, Forschung und Technologie (Fö. 01KS9602) and the Interdisziplinäres Zentrum für Klinische Forschung der Universität Tübingen (IZKF) (S. 05.00023.2/IIB9) and of the fortune program, Tübingen. This work was also supported by NIH grant HL58398.

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Correspondence to Florian Lang.

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Ullrich, S., Berchtold, S., Boehmer, C. et al. Pseudomonas aeruginosa activates Cl channels in host epithelial cells. Pflugers Arch - Eur J Physiol 447, 23–28 (2003). https://doi.org/10.1007/s00424-003-1136-6

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  • DOI: https://doi.org/10.1007/s00424-003-1136-6

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