Toll‐like receptor 4 ligand can differentially modulate the release of cytokines by human platelets
Résumé
Toll-like receptor 4 ligand can differentially modulate the release of cytokines by human platelets Lipopolysaccharide (LPS), a cell wall component of all Gramnegative bacteria, is composed of an amphipathic lipid A moiety, core oligosaccharides and a variable O-antigen polysaccharide domain. It is the natural ligand for Toll-like receptor 4 (TLR4), the presence of which is essential for the cell response to LPS. A link between TLR4 and innate immunity has been described (Cook et al, 2004). The recognition of LPS by the innate immune system results in an inflammatory response characterized by the production of cytokines, such as tumour necrosis factor alpha, interleukin (IL)-1b, IL-6 and IL-8 (Akira & Takeda, 2004). Thus, TLR4 appears to be an important factor for the detection of pathogens and the induction of an adaptive immune response (Medzhitov et al, 1997).
Blood platelets, which are central to haemostasis, also have profound effects on the regulation of the immune system, linking innate (including inflammation) and adaptative immunity (Tang et al, 2002; Elzey et al, 2003; Yeaman & Bayer, 2006; von Hundelshausen & Weber, 2007). Furthermore, several studies have implicated LPS as a modulator of platelet function. Shibazaki et al (1996) showed that LPS from Escherichia coli induces a biphasic, organ-and strain-specific accumulation of murine platelets, and proposed that this effect is involved in the development of septic shock. Endo and
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