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Differential regulation of Moraxella catarrhalis-induced interleukin-8 response by protein kinase C isoforms

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

CORRESPONDENCE: H. Slevogt, Dept of Internal Medicine/Infectious Diseases and Respiratory Medicine, Charité – Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. Fax: 49 30450553906. E-mail: hortense.slevogt{at}charite.de

Keywords: Cytokine response, Moraxella catarrhalis, protein kinase C isoforms, pulmonary epithelial cells, ubiquitous surface protein A2

Received: August 9, 2007
Accepted December 11, 2007

Moraxella catarrhalis is a major cause of infectious exacerbations of chronic obstructive lung disease. In pulmonary epithelial cells, M. catarrhalis induces release of the pro-inflammatory cytokine interleukin (IL)-8, which plays a pivotal role in orchestrating airway inflammation.

The present study demonstrated that protein kinase (PK)C was activated by Moraxella infection and positively regulated M. catarrhalis-triggered nuclear factor (NF)-B activation and subsequent IL-8 release. Activation of the PKC/NF-B signalling pathway was found to be dependent on expression of the Moraxella-specific ubiquitous surface protein A2. In addition, it was shown that specific isoforms of PKC play differential roles in the fine-tuning of the M. catarrhalis-induced NF-B-dependent gene expression through controlling il8 promoter activity. Inhibition of PKC and with chemical inhibitors or using short interfering RNA-mediated gene silencing significantly suppressed, whereas inhibition of PKC increased, the M. catarrhalis-induced IL-8 transcription and cytokine release.

In conclusion, it was shown that Moraxella catarrhalis infection activates protein kinase C and its isoforms , and , which differentially regulate interleukin-8 transcription in human pulmonary epithelial cells.