Platelet responses and anaphylaxis‐like shock induced in mice by intravenous injection of whole cells of oral streptococci

Abstract

Intravenous injection of lyophilized whole cells of various oral streptococcal strains into muramyldipeptide (MDP)-primed C3H/HeN mice induces rapid anaphylactoid shock. Here we examined the mechanism underlying this shock. In non-primed mice, Streptococcus intermedius K-213K (SiK213) and Streptococcus constellatus T21 (ScT21) produced little or no sign of shock. In MDP-primed mice, SiK213 caused lethal shock, while ScT21 only had a weak effect. SiK213 induced decreases in blood platelets and 5-hydroxytryptamine (5HT) preceding the shock, while the effects of ScT21 were weak. The SiK213-induced 5HT decrease and shock were reduced by a complement-C5 inhibitor. These results suggest that (i). streptococcal bacterial cells can induce rapid platelet responses, (ii). complement-dependent degradation of platelets may be involved in streptococcus-induced shock, (iii). the streptococcus-induced platelet degradation or degranulation may occur largely in the systemic circulation, and (iv). platelets may play a role not only in infectious diseases caused by gram-negative bacteria, but also in diseases caused by gram-positive bacteria.

Histone-like DNA binding protein of Streptococcus intermedius induces the expression of pro-inflammatory cytokines in human monocytes via activation of ERK1/2 and JNK pathways

“…In combination with agonists for TLR2, TLR4 and TLR9, MDP induced marked synergistic pro-inflammatory cytokine secretion in human monocytic cells (Yang et al, 2001;Fritz et al, 2005;Uehara et al, 2005). Moreover, MDP-primed mice were hypersensitive to intravenous injections of Salmonella LPS and lyophilized whole cells of S. intermedius or S. constellatus (Takada and Galanos, 1987;Ohba et al, 2004). A recent report showing that the incubation of cells with MDP alone caused a significant expression of TNF-a mRNA but minimal production of TNF-a suggested that the majority of TNF-a mRNA induced by MDP alone is not translated into protein (Wolfert et al, 2002).…”

Platelet Toll-like receptor expression modulates lipopolysaccharide-induced thrombocytopenia and tumor necrosis factor-α production in vivo

“…32,33 LPS has also been shown to inhibit human platelet aggregation stimulated by agonists by inhibiting phosphoinositide breakdown and intracellular Ca ϩϩ mobilization. 34 Furthermore, LPS triggers the production of several proinflammatory cytokines (eg, TNF, IL-1) and the adherence of monocytes to endothelial cells.…”

Pharmacological characterization of anaphylaxis-like shock responses induced in mice by mannan and lipopolysaccharide

“…Injection of whole cells of streptococci (Gram-positive bacteria) also induces ALS [8]. Interestingly, the induction of both LPS-ALS and Streptococcus-ALS involves activation of platelets followed by their degradation in the lung, liver, and/or circulation [9,10], and this platelet response is induced by activation of the lectin pathway in the complement system [8,11,12]. In the Klebsiella O3 LPS molecule, the mannose homopolymer structure within the O-antigen region is important for stimulation of the lectin pathway [12].…”

“…Pretreatment with MDP augments both LPS-ALS and endotoxin shock in mice, including C3H/HeJ mice [1,2,7]. Injection of whole cells of streptococci (Gram-positive bacteria) also induces ALS [8]. Interestingly, the induction of both LPS-ALS and Streptococcus-ALS involves activation of platelets followed by their degradation in the lung, liver, and/or circulation [9,10], and this platelet response is induced by activation of the lectin pathway in the complement system [8,11,12].…”