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Porphyromonas gingivalis modulates Pseudomonas aeruginosa-induced apoptosis of respiratory epithelial cells through the STAT3 signaling pathway. - PubMed - NCBI
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Microbes Infect. 2014 Jan;16(1):17-27. doi: 10.1016/j.micinf.2013.10.006. Epub 2013 Oct 16.

Porphyromonas gingivalis modulates Pseudomonas aeruginosa-induced apoptosis of respiratory epithelial cells through the STAT3 signaling pathway.

Author information

1
Department of Oral Biology and Periodontics, School of Stomatology, China Medical University, Nanjing North St. 117, Shenyang 110002, Liaoning Province, China.
2
Department of Oral Biology, School of Dental Medicine, 109 Foster Hall, University at Buffalo, State University of New York, 3435 Main St., Buffalo, NY 14214-3092, USA.
3
Department of Oral Biology and Periodontics, School of Stomatology, China Medical University, Nanjing North St. 117, Shenyang 110002, Liaoning Province, China; Department of Oral Biology, School of Dental Medicine, 109 Foster Hall, University at Buffalo, State University of New York, 3435 Main St., Buffalo, NY 14214-3092, USA. Electronic address: yppan@mail.cmu.edu.cn.

Abstract

Pseudomonas aeruginosa is an important opportunistic bacterial pathogen, causing infections of respiratory and other organ systems in immunocompromised hosts that may invade and proliferate in mucosal epithelial cells to induce apoptosis. Previous studies suggest that oral bacteria, especially gram-negative periodontal pathogens, may enhance P. aeruginosa invasion into respiratory epithelial cells to augment tissue destruction. In this study, we investigated the effect of the periodontopathogen Porphyromonas gingivalis on P. aeruginosa-induced epithelial cell apoptosis. P. gingivalis invasion transiently inhibited P. aeruginosa-induced apoptosis in respiratory epithelial cells via the signal transducer and activator of transcription 3 (STAT3) signaling pathway. The activated STAT3 up-regulated the downstream anti-apoptotic moleculars survivin and B-cell leukemia-2 (bcl-2). This process was accompanied by down-regulation of pro-apoptosis molecular Bcl-2-associated death promoter (bad) and caspase-3 activity inhibition. In addition, the activation of the STAT3 pathway was affected by P. gingivalis in a dose-dependent manner. Finally, co-invasion of P. aeruginosa and P. gingivalis led to greater cell death compared with P. aeruginosa challenge alone. These results suggest that regulation of P. aeruginosa-induced apoptosis by P. gingivalis contributes to the pathogenesis of respiratory disease. Interference with this process may provide a potential therapeutic strategy for the treatment and prevention of respiratory disease.

KEYWORDS:

Apoptosis; Porphyromonas gingivalis; Pseudomonas aeruginosa; Respiratory infection; Signal transduction pathway

PMID:
24140557
DOI:
10.1016/j.micinf.2013.10.006
[Indexed for MEDLINE]
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