PT  - JOURNAL ARTICLE
AU  - H. Slevogt
AU  - L. Maqami
AU  - K. Vardarowa
AU  - W. Beermann
AU  - A. C. Hocke
AU  - J. Eitel
AU  - B. Schmeck
AU  - A. Weimann
AU  - B. Opitz
AU  - S. Hippenstiel
AU  - N. Suttorp
AU  - P. D. N'Guessan
TI  - Differential regulation of <em>Moraxella catarrhalis</em>-induced interleukin-8 response by protein kinase C isoforms
AID  - 10.1183/09031936.00103507
DP  - 2008 Apr 01
TA  - European Respiratory Journal
PG  - 725--735
VI  - 31
IP  - 4
4099  - http://erj.ersjournals.com/content/31/4/725.short
4100  - http://erj.ersjournals.com/content/31/4/725.full
SO  - Eur Respir J2008 Apr 01; 31
AB  - 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)-κB activation and subsequent IL-8 release. Activation of the PKC/NF-κB 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-κB-dependent gene expression through controlling il8 promoter activity. Inhibition of PKCα and ϵ with chemical inhibitors or using short interfering RNA-mediated gene silencing significantly suppressed, whereas inhibition of PKCθ 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 α, ϵ and θ, which differentially regulate interleukin-8 transcription in human pulmonary epithelial cells.