Intravenous injection of specified bacterial lipopolysaccharides (LPSs) induced anaphylactoid shock in mice of various strains, including LPS-resistant C3H/HeJ. The reaction was accompanied by occasional mortality of mice within 1 h. Prior to shock, rapid accumulation of blood platelets in the lungs and liver followed by degradation of platelets (or release of their contents) and tissue destruction were observed. In this study, LPS specimens carrying mannose-homopolymer (MHP), which markedly activate the human complement system through the lectin pathway, induced marked platelet degradation and anaphylactoid shock in BALB/c mice. In contrast, in C5-deficient DBA/2 mice, the platelet degradation and anaphylactoid reactions did not occur. Anti-complement agent K-76 COOH (C5 inhibitor) protected BALB/c mice from mortality in the anaphylactoid reaction. K-76 COOH also inhibited platelet degradation, but not accumulation, induced by LPS in mice. Based on these findings, we postulated that strong complement activation by specified LPS preparations induced degradation of platelets that have accumulated in the lungs and liver, resulting in acute inflammation accompanied by severe tissue destruction, especially in the lungs, which in turn leads to anaphylactoid reaction.
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