Journal
EXPERIMENTAL LUNG RESEARCH
Volume 38, Issue 2, Pages 100-110Publisher
TAYLOR & FRANCIS INC
DOI: 10.3109/01902148.2011.652802
Keywords
AP-1; beta-defensins; kinases; NF-kappa B; Streptococcus pneumoniae; TLR2
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Funding
- Deutsche Forschungsgemeinschaft [DFG-SFB TRR84]
- Bundesministerium fur Bildung und Forschung (BMBF Network PROGRESS)
- Charite-Universitatsmedizin Berlin
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Streptococcus pneumoniae is an important causative agent of pneumonia in humans. Pulmonary epithelial surfaces constitutes not only a mechanical barrier against invading pathogens but also essentially contribute to innate immunity by producing antimicrobial peptides such as human beta-defensin-2 (hBD-2) and -3 (hBD-3). In this study the authors demonstrated that pneumococci induced hBD-2 and hBD-3 expression in human pulmonary epithelial cells. Further analysis indicated an essential role of Toll-like receptor 2 (TLR2) for the expression of both peptides in infected pulmonary epithelial cells. Whereas the hBD-2 release was controlled by the phosphoinositide 3-kinase (PI3K) and the transcription factor nuclear factor kappa B (NF-kappa B), hBD-3 was triggered via the c-Jun N-terminal kinase (JNK)-activator protein 1 (AP-1) pathway. Additionally, the authors showed that exogenous hBD-2 as well as hBD-3 elicited a strong antimicrobial effect on S. pneumoniae. Thus, differential regulation of the expression of hBD-2 and hBD-3 might play an important role in pneumococci pneumonia.
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