2012
DOI: 10.1016/j.clim.2012.09.004
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Human platelets can discriminate between various bacterial LPS isoforms via TLR4 signaling and differential cytokine secretion

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Cited by 124 publications
(139 citation statements)
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“…E. coli LPS did result in increased PS positivity. Previous studies have also shown that platelets can react differently to various forms of LPS, and suggested that this might be due to differences in TLR4 and CD14 binding (29) or structure of the O-antigen region of LPS and activation of the lectin pathway of the complement system (30). Platelets do not express CD14, but can absorb large amounts from plasma (31), which might also play a role in our results -as stimulations were performed in platelet rich plasma.…”
Section: Discussionmentioning
confidence: 99%
“…E. coli LPS did result in increased PS positivity. Previous studies have also shown that platelets can react differently to various forms of LPS, and suggested that this might be due to differences in TLR4 and CD14 binding (29) or structure of the O-antigen region of LPS and activation of the lectin pathway of the complement system (30). Platelets do not express CD14, but can absorb large amounts from plasma (31), which might also play a role in our results -as stimulations were performed in platelet rich plasma.…”
Section: Discussionmentioning
confidence: 99%
“…CD14 is a glycoprotein located on the cell surface and is mainly produced by monocytes, macrophages, and neutrophils (Parajuli et al, 2012). CD14 has been shown to be involved in primary immune and inflammatory responses (Apetoh et al, 2007;Berthet et al, 2012;Guo et al, 2013). Studies have demonstrated that genetic variations in CD14 may change the structure of the CD14 protein and influence CD14-lipopolysaccharide (LPS) interactions (Baldini et al, 1999;Karhukorpi et al, 2002).…”
Section: Introductionsmentioning
confidence: 99%
“…Les plaquettes, qui expriment des Toll-like receptors ou TLR [33] peuvent aussi lier des dérivés microbiens bactériens, viraux ou parasitaires, qui activent ces cellules (pourvues d'un inflammasome), et qui déclenchent la sécrétion différenciée de cytokines pro-inflammatoires, selon des programmes ressemblant aux programmes de différenciation des cellules nucléées [20,34]. Le sepsis (grande manifestation inflammatoire) est un bon exemple de ces interactions complexes entre les plaquettes et les agents infectieux [35,36].…”
Section: Agents Infectieux Ou Leurs Produits De Dégradationunclassified