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Effect of C3 depletion on the genesis of thrombocytopenia induced in rats by Erysipelothrix rhusiopathiae
Author(s) -
Nakato Hidekazu,
Shinomiya Keisuke,
Mikawa Haruki
Publication year - 1986
Publication title -
scandinavian journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0036-553X
DOI - 10.1111/j.1600-0609.1986.tb01766.x
Subject(s) - erysipelothrix rhusiopathiae , platelet , chemistry , egta , platelet rich plasma , magnesium , calcium , saline , microbiology and biotechnology , acetic acid , pathogenesis , biochemistry , immunology , endocrinology , biology , organic chemistry
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 veronalbuffered 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.