Porphyromonas gingivalis enhances pneumococcal adhesion to human alveolar epithelial cells by increasing expression of host platelet-activating factor receptor

FEBS Letters

article

Noriaki Kamio¹  Mayumi Hayata¹  Muneaki Tamura¹  Hajime Tanaka¹  Kenichi Imai¹ 

[1] Department of Microbiology, Nihon University School of Dentistry

关键词: adhesion;    alveoli;    gingipain;    lung;    PAFR;    platelet-activating factor receptor;    pneumonia;    Porphyromonas gingivalis;    Streptococcus pneumoniae;   

DOI  :  10.1002/1873-3468.14084

来源: John Wiley & Sons Ltd.

【 摘 要 】

Streptococcus pneumoniae causes pneumonia by infecting the alveolar epithelium via binding to host receptors, such as the platelet-activating factor receptor (PAFR). Although chronic periodontitis has been identified as a pneumonia risk factor, how periodontopathic bacteria cause pneumonia is not known. We found that S. pneumoniae adhered to PAFR expressed on A549 human alveolar epithelial cells stimulated by Porphyromonas gingivalis culture supernatant, and this was abrogated by a PAFR-specific inhibitor. Among the major virulence factors of P .  gingivalis [lipopolysaccharide (LPS), fimbriae and gingipains (Rgps and Kgp)], PAFR expression and pneumococcal adhesion were executed in an Rgp-dependent manner. LPS and fimbriae did not induce PAFR expression. Hence, our findings suggest that P .  gingivalis enhances pneumococcal adhesion to human alveoli by inducing PAFR expression and that gingipains are responsible for this.

【 授权许可】

Unknown