PMID: 3764331Jul 1, 1986Paper

Effect of C3 depletion on the genesis of thrombocytopenia induced in rats by Erysipelothrix rhusiopathiae

Scandinavian Journal of Haematology
H NakatoH Mikawa

Abstract

The role of complement in the pathogenesis of marked thrombocytopenia induced in rats by Erysipelothrix rhusiopathiae (E. rhusiopathiae) was examined. In cobra venom factor (CoF)-treated rats thrombocytopenia was not induced by the bacterium. The content of 5-hydroxytryptamine (5-HT) in platelets was decreased significantly after inoculation only in untreated rats. E. rhusiopathiae could bind C3 and generate platelet-bacteria aggregation when incubated in the plasma diluted with veronal-buffered saline containing calcium and magnesium (VBS++) or gelatin-VBS containing magnesium and ethyleneglycol tetra-acetic acid (GVB-Mg-EGTA), but not when incubated in GVB-ethylenediamine tetra-acetic acid (GVB-EDTA) diluted plasma or in CoF-treated or anti rat C3-treated plasma. When platelets were preincubated with activated zymosan, no bacteria could bind to platelets. From the results, we speculate that the alternative complement pathway, activated by E. rhusiopathiae, appears to mediate the formation of platelet-bacterial aggregations that may accelerate the removal of platelets from circulating blood.

References

Aug 1, 1977·Infection and Immunity·C G StephensW P Reed
Mar 1, 1976·The Journal of Surgical Research·L OppenheimerA J Bishop
Jan 1, 1985·Experimental Pathology·H NakatoH Mikawa
Feb 1, 1972·British Journal of Haematology·J F MustardM A Packham
Sep 1, 1965·Immunochemistry·G ManciniJ F Heremans
Jul 1, 1982·Seminars in Thrombosis and Hemostasis·J J WilsonJ G Kelton

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