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Inhibitory effects of azithromycin on the adherence ability of Porphyromonas gingivalis
Author(s) -
Kan Powen,
Sasaki Haruka,
Inaba Keitaro,
Watanabe Kiyoko,
Hamada Nobushiro,
Minabe Masato
Publication year - 2019
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1002/jper.18-0559
Subject(s) - porphyromonas gingivalis , microbiology and biotechnology , azithromycin , fimbria , hemagglutinin (influenza) , bacteroidaceae , blot , minimum inhibitory concentration , biology , gel electrophoresis , bacteria , chemistry , virulence , antibiotics , antibody , immunology , biochemistry , genetics , gene
Background Porphyromonas gingivalis is a major pathogen and has a high detection rate in periodontal disease. Fimbriae and hemagglutinin are expressed by P. gingivalis , and these play an important role in the adherence of the bacteria to periodontal tissue and biofilm formation. The aim of this study was to investigate the effects of sub‐minimal inhibitory concentrations (sub‐MICs) of azithromycin on the adherence of P. gingivalis , focusing on the inhibition of fimbriae expression and hemagglutinin activity. Methods P. gingivalis ATCC 33277 were incubated anaerobically with sub‐MICs of azithromycin at 37°C by gentle shaking for 18 hours. The bacterial cells were harvested, washed twice with phosphate‐buffered saline (PBS), and the proteins analyzed by 12% sodium dodecyl sulfate‐polyacrylamide gel electrophoresis (SDS‐PAGE) and western blotting. Adherence assay and hemagglutinin activity tests were done with the same culture. Results The results of SDS‐PAGE indicated that the sub‐MICs of azithromycin inhibited 41‐kDa fimbrial protein expression and hemagglutinin activities. The disappearance of 41‐kDa fimbrial protein expression and long fimbriae in 0.4 µg/mL, 0.2 µg/mL, and 0.1 µg/mL of azithromycin was confirmed by western blotting and transmission electron microscopy. The adherence of P. gingivalis to human gingival epithelial cells was reduced by sub‐MICs of azithromycin compared with the adherence levels without antibiotic. Conclusions These results suggest that sub‐MICs of azithromycin may reduce the adherence of P. gingivalis to host cells, by inhibiting production of fimbriae and hemagglutinin activities. Therefore, azithromycin can be used as a biofilm treatment of periodontal disease caused by P. gingivalis .