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Background   Porphyromonas gingivalis  ( P. gingivalis ), one of the main pathogenic bacteria involved in periodontitis, induces the expression of intercellular adhesion molecule − 1 (ICAM-1) and monocyte-endothelial cell adhesion. This effect plays a pivotal role in atherosclerosis development. Macrophage migration inhibitory factor (MIF) is a multifunctional cytokine and critically affects atherosclerosis pathogenesis. In this study, we tested the involvement of MIF in the  P. gingivalis  ATCC 33277-enhanced adhesive properties of endothelial cells.    Results  Endothelial MIF expression was enhanced by  P. gingivalis  ATCC 33277 infection. The MIF inhibitor ISO-1 inhibited ICAM-1 production in endothelial cells, and monocyte-endothelial cell adhesion was induced by  P. gingivalis  ATCC 33277 infection. However, the addition of exogenous human recombinant MIF to  P. gingivalis  ATCC 33277-infected endothelial cells facilitated monocyte recruitment by promoting ICAM-1 expression in endothelial cells.    Conclusions  These experiments revealed that MIF in endothelial cells participates in the pro-atherosclerotic lesion formation caused by  P. gingivalis  ATCC 33277 infection. Our novel findings identify a more detailed pathological role of  P. gingivalis  ATCC 33277 in atherosclerosis.

bmc microbiology

Porphyromonas gingivalis ATCC 33277 promotes intercellular adhesion molecule-1 expression in endothelial cells and monocyte-endothelial cell adhesion through macrophage migration inhibitory factor