TY - JOUR
T1 - Adhesion and invasion of gingival epithelial cells by Porphyromonas gulae
AU - Inaba, Hiroaki
AU - Nomura, Ryota
AU - Kato, Yukio
AU - Takeuchi, Hiroki
AU - Amano, Atsuo
AU - Asai, Fumitoshi
AU - Nakano, Kazuhiko
AU - Lamont, Richard J.
AU - Matsumoto-Nakano, Michiyo
N1 - Funding Information:
This research was supported by grants-in-aid for Scientific Research (17K11612 to H.I., A26253094 to A.A., 30359848 to M.M.N.) from the Ministry of Education, Culture, Sports, Science and Technology; to H.I. from Ryobi Teien Memory Foundation; and DE011111 and DE017921 to R.J. L. from the NIH.
Publisher Copyright:
© 2019 Inaba et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2019/3
Y1 - 2019/3
N2 - Porphyromonas gulae, an animal periodontal pathogen, possess fimbriae classified into three genotypes (A-C) based on the diversity of fimA genes encoding FimA. Accumulating evidence suggests that P. gulae strains with type C fimbriae are more virulent as compared to those with other types. The ability of these organisms to adhere to and invade gingival epithelial cells has yet to be examined. P. gulae showed the greatest levels of adhesion and invasion at a multiplicity of infection of 100 for 90 min. P. gulae type C and some type B strains invaded gingival epithelial cells at significantly greater levels than the other strains, at the same level of efficiency as P. gingivalis with type II fimbriae. Adhesion and invasion of gingival epithelial cells by P. gulae were inhibited by cytochalasin D and sodium azide, indicating the requirements of actin polymerization and energy metabolism for those activities. Invasion within gingival epithelial cells was blocked by staurosporine, whereas those inhibitors showed little effects on adhesion, while nocodazole and cycloheximide had negligible effects on either adhesion or invasion. P. gulae proteases were found to be essential for adhesion and invasion of gingival epithelial cells, while its DNA and RNA, and protein synthesis were unnecessary for those activities. Additionally, α5β1 integrin antibodies significantly inhibited adhesion and invasion by P. gulae. This is the first report to characterize P. gulae adhesion and invasion of human gingival epithelial cells.
AB - Porphyromonas gulae, an animal periodontal pathogen, possess fimbriae classified into three genotypes (A-C) based on the diversity of fimA genes encoding FimA. Accumulating evidence suggests that P. gulae strains with type C fimbriae are more virulent as compared to those with other types. The ability of these organisms to adhere to and invade gingival epithelial cells has yet to be examined. P. gulae showed the greatest levels of adhesion and invasion at a multiplicity of infection of 100 for 90 min. P. gulae type C and some type B strains invaded gingival epithelial cells at significantly greater levels than the other strains, at the same level of efficiency as P. gingivalis with type II fimbriae. Adhesion and invasion of gingival epithelial cells by P. gulae were inhibited by cytochalasin D and sodium azide, indicating the requirements of actin polymerization and energy metabolism for those activities. Invasion within gingival epithelial cells was blocked by staurosporine, whereas those inhibitors showed little effects on adhesion, while nocodazole and cycloheximide had negligible effects on either adhesion or invasion. P. gulae proteases were found to be essential for adhesion and invasion of gingival epithelial cells, while its DNA and RNA, and protein synthesis were unnecessary for those activities. Additionally, α5β1 integrin antibodies significantly inhibited adhesion and invasion by P. gulae. This is the first report to characterize P. gulae adhesion and invasion of human gingival epithelial cells.
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U2 - 10.1371/journal.pone.0213309
DO - 10.1371/journal.pone.0213309
M3 - Article
C2 - 30870452
AN - SCOPUS:85062945160
SN - 1932-6203
VL - 14
JO - PLoS One
JF - PLoS One
IS - 3
M1 - e0213309
ER -