Source: Annual Congress 2008 - Mechanisms of respiratory infections: interaction between the pathogen and the host
Disease area: Airway diseases, Respiratory infections

Abstract

Moraxella catarrhalis is a major cause of infectious exacerbations of chronic obstructive lung disease (COPD). Antimicrobial peptides secreted by pulmonary epithelium are essential components of the innate immune response of the human lung. Beta defensine 3 (hBD3) has been shown to play a key role in chronic inflammatory lung diseases. For some pathogens, hBD3 induces a strong antimicrobial activity. The goal of this study was to investigate antimicrobial properties of hBD3 on Moraxella catarrhalis and to determine the effect of this pathogen on hBD3 expression in lung epithelium. Moreover the signaling pathways involved in this process has been characterized.
Results: Incubation of M. catarrhalis with recombinant hBD3 showed a strong antimicrobial effect. Furthermore infection of human bronchial epithelial cells with M. catarrhalis, increased the transcription and the release of hBD3. Expression of hBD3 was mediated through Lipooligosaccharide (LOS) dependent activation of TLR2, ERK 1/2- and JNK pathways. Additionally incubation of the cells with the Hag deletion mutant of M. catarrhalis strongly reduced the peptide expression, suggesting an important role of this M. catarrhalis specific virulence factor for hBD3.
Pre-incubation of bronchial epithelial cells with the classic COPD medication dexamethason but not with Theophyllin inhibited M. catarrhalis-induced hBD3 release.
Conclusion: M. catarrhalis induced TLR2, ERK 1/2- and JNK dependent expression of hBD3 which could be suppressed by Dexamethason. These observations may be essential for the specific interactions of M. catarrhalis with the human pulmonary mucosa in the course of COPD.

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P. D. N‘Guessan, T. Steiner, S. Scharf, H. Helge, B. Opitz, J. Eitel, S. Hippenstiel, N. Suttorp, H. Slevogt (Berlin, Germany). Role and regulation of moraxella catarrhalis-induced beta defensin 3 expression in human pulmonary epithelial cells. Eur Respir J 2008; 32: Suppl. 52, 2289

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