| 摘要: | 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 jB 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 |
