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Porphyromonas gingivalis enhances pneumococcal adhesion to human alveolar epithelial cells by increasing expression of host platelet‐activating factor receptor
Author(s) -
Kamio Noriaki,
Hayata Mayumi,
Tamura Muneaki,
Tanaka Hajime,
Imai Kenichi
Publication year - 2021
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.14084
Subject(s) - platelet activating factor receptor , porphyromonas gingivalis , fimbria , streptococcus pneumoniae , microbiology and biotechnology , virulence factor , bacterial adhesin , lipopolysaccharide , platelet activating factor , receptor , chemistry , biology , immunology , virulence , bacteria , biochemistry , gene , antagonist , antibiotics , genetics
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.