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Porphyromonas gingivalis fimbriae‐dependent interleukin‐6 autocrine regulation by increase of gp130 in endothelial cells
Author(s) -
Ho YS.,
Lai MT.,
Liu SJ.,
Lin CT.,
Naruishi K.,
Takashiba S.,
Chou HH.
Publication year - 2009
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.2008.01150.x
Subject(s) - porphyromonas gingivalis , fimbria , biology , autocrine signalling , human umbilical vein endothelial cell , microbiology and biotechnology , endothelium , interleukin , umbilical vein , immunology , cytokine , cell culture , in vitro , endocrinology , escherichia coli , bacteria , gene , biochemistry , genetics
Background and Objective: Local persistent infection by Porphyromonas gingivalis leads to inflammatory systemic diseases, such as atherosclerosis. We have reported previously that avirulent P. gingivalis fimbriae‐dependent invasion into endothelial cells might be involved in progression of atherosclerosis. Although interleukin‐6 (IL‐6) regulates progression of atherosclerosis, little is known about the relationship of P. gingivalis fimbriae‐dependent invasion to IL‐6 regulation in endothelial cells. Material and Methods: We examined the secretion of IL‐6 and the expression of the IL‐6 signal transducer gp130 in human umbilical vein endothelial cells (HUVEC) infected with the wild‐type FDC381 strain of P. gingivalis and a fimbriae‐deficient mutant ( fimA ) by enzyme‐linked immunosorbent assay, quantitative reverse transcriptase‐polymerase chain reaction (RT‐PCR) and flow cytometry (fluorescence‐activated cell sorting, FACS) analysis. Results: Coculture of HUVEC with P. gingivalis resulted in increase of IL‐6 secretion at 24 h postinfection. Interestingly, the increase was inhibited significantly in HUVEC infected with the P. gingivalis fimA mutant. In addition, the increase of IL‐6 secretion induced by P. gingivalis infection was significantly impaired by the meiosis specific kinase 1 inhibitor, PD98059, or the nuclear factor κB inhibitor, Bay11‐7082. Furthermore, we demonstrated that gp130 expression increased with P. gingivalis infection. Importantly, gp130 expression was significantly impaired by P gingivalis fimA mutant infection compared with wild‐type P. gingivalis infection, as assessed by both quantitative RT‐PCR and FACS analysis. Conclusion: Our findings indicate that P. gingivalis fimbriae are important factors in the autocrine regulation of IL‐6, by increasing gp130 in endothelial cells.