Background:
@EN Tissue type plasminogen activator(tPA), type 1 plasminogen activatot inhibitor (PAI-1), and von Willebrand factor ar known to be released into the sera of patients in disseminated intravascular coagulation(DIC). The main pathologic mechanism
of
tsutsugamushi disease is the vasculitis by direct endothelial cell invasion by R. tsutsugamushi which dosen't have endotoxin. It is suspected that the mechanisms of DIC and activation of plasminogen activation system are different from those of
sepsis
by other organisms, which is caused by endotoxin. We suspect that direct rickettsial invasion of endothelial cells causes endothelial cell damage, tissue factor release, which is followed by DIC, and tPA and PAI-1 are released as compensatory
mechanism.
@ES Methods:
@EN We cultured endothelial cells from human umbilical cord vein, infected them with purified R. tsutsugamushi Gilliam strain, checked tPA and PAI-1 by ELISA in culture supernatant. Then we observed the tissue factor expression on cultured
endothelial
cell monolayer by indirect IF stain. PAI-1 gene expression was evaluated by northern blot analysis.
@ES Results:
@EN: 1) PAI-1 level showed gradual increase up to 240ng/ml (2.5-4.7 fold increase) in 24 hours.
2) tPA level showed no significant change with time.
3) PAI-1 gene expression increased 2.5 fold by northern blot analysis.
4) Tissue factor was expressed on the endothelial cells infected with R. tsutsugamushi.
@ES Conclusion:
@EN R. tsutsugamushi infection induces expression of tissue factor on endothelial cells and PAI-1 synthesis and it would contribute to DIC mechanism in tsutsugamushi disease in part. But it has no direct effect on tPA release.
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