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Published online before print January 9, 2008
Eur Respir J 2008, doi:10.1183/09031936.00103507
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ORIGINAL ARTICLE

Differental regulation of Moraxella catarrhalis-induced IL-8 response by PKC isoforms

H. Slevogt 1*, L. Maqami 1, K. Vardarowa 1, W. Beermann 1, A.C. Hocke 1, J. Eitel 1, B. Schmeck 1, A. Weimann 2, B. Opitz 1, S. Hippenstiel 1, N. Suttorp 1, P.D. N'Guessan 1

1 Dept of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité – Universitätsmedizin Berlin, 13353 Berlin, Germany
2 Institute of Laboratory Medicine and Biochemistry, Charité – Universitätsmedizin Berlin, 13353 Berlin, Germany

* To whom correspondence should be addressed. E-mail: hortense.slevogt{at}charite.de.


  Abstract

Moraxella catarrhalis is a major cause of infectious exacerbations of chronic obstructive lung disease (COPD). In pulmonary epithelial cells, M. catarrhalis induces release of the pro-inflammatory cytokine interleukin 8 (IL-8) which plays a pivotal role in orchestrating airway inflammation. Herein we demonstrate that protein kinase C (PKC) is activated by Moraxella infection and positively regulated M. catarrhalis- triggered NF-{kappa}B activation and subsequent IL-8 release. Activation of the PKC/NF-{kappa}B signaling pathway was found to be dependent on expression of the Moraxella-specific ubiquitous surface protein (Usp) A2. In addition, we show that specific isoforms of PKC play differential roles in fine tuning of the M. catarrhalis-induced NF-{kappa}B-dependent gene expression through controlling il8 promoter activity. Inhibition of PKC{alpha} and {epsilon} with chemical inhibitors or using siRNA-mediated gene silencing significantly suppressed, whereas inhibition of PKC{theta} increased the M. catarrhalis-induced IL-8 transcription and cytokine release. In conclusion, we show that M. catarrhalis infection activates PKC and its isoforms {alpha}, {epsilon} and {theta} which are differentially regulating IL-8 transcription in human pulmonary epithelial cells.

Keywords:  Cytokine response, Moraxella catarrhalis, PKC isoforms, pulmonary epithelial cells, UspA2




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