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Suppression of inflammatory responses of human gingival fibroblasts by gingipains from Porphyromonas gingivalis
Author(s) -
Palm E.,
Khalaf H.,
Bengtsson T.
Publication year - 2015
Publication title -
molecular oral microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.18
H-Index - 77
eISSN - 2041-1014
pISSN - 2041-1006
DOI - 10.1111/omi.12073
Subject(s) - porphyromonas gingivalis , microbiology and biotechnology , proteases , slpi , chemistry , immune system , virulence , periodontitis , secretion , virulence factor , chronic periodontitis , immunology , inflammation , biology , medicine , enzyme , gene , biochemistry
Summary The interaction between human gingival fibroblasts ( HGF s) and Porphyromonas gingivalis plays an important role in the development and progression of periodontitis. Porphyromonas gingivalis possesses several virulence factors, including cysteine proteases, the arginine‐specific (Rgp) and lysine‐specific (Kgp) gingipains. Studying the mechanisms that P. gingivalis , and its derived virulence, use to propagate and interact with host cells will increase the understanding of the development and progression of periodontitis. In this study, we aimed to elucidate how P. gingivalis influences the inflammatory events in HGF s regarding transforming growth factor‐β 1 ( TGF ‐β 1 ), CXCL 8, secretory leucocyte protease inhibitor ( SLPI ), c‐Jun and indoleamine 2,3‐dioxygenase ( IDO ). HGF s were inoculated for 6 and 24 h with the wild‐type strains ATCC 33277 and W50, two gingipain‐mutants of W50 and heat‐killed ATCC 33277. The P. gingivalis regulated CXCL 8 and TGF ‐β 1 in HGF s, and the kgp mutant gave significantly higher immune response with increased CXCL 8 ( P < 0.001) and low levels of TGF ‐β 1 . We show that HGF s express and secrete SLPI , which was significantly suppressed by P. gingivalis ( P < 0.05). This suggests that by antagonizing SLPI , P. gingivalis contributes to the tissue destruction associated with periodontitis. Furthermore, we found that P. gingivalis inhibits the expression of the antimicrobial IDO , as well as upregulating c‐Jun ( P < 0.05). In conclusion, P. gingivalis both triggers and suppresses the immune response in HGF s. Consequently, we suggest that the pathogenic effects of P. gingivalis , and especially the activity of the gingipains on the inflammatory and immune response of HGF s, are crucial in periodontitis.