title: Human platelets can discriminate between various bacterial LPS isoforms via TLR4 signaling and differential cytokine secretion.
abstract: Platelets are currently acknowledged as cells of innate immunity and inflammation and play a complex role in sepsis. We examined whether different types of LPS have different effects on the release of soluble signaling/effective molecules from platelets. We used platelet-rich plasma from healthy volunteers and LPS from two strains of gram-negative bacteria with disparate LPS structures. We combined LPS-stimulated platelet supernatants with reporter cells and measured the PBMC cytokine secretion profiles. Upon stimulation of platelets with both Escherichia coli O111 and Salmonella minnesota LPS, the platelet LPS::TLR4 interaction activated pathways to trigger the production of a large number of molecules. The different platelet supernatants caused differential PBMC secretion of IL-6, TNFα, and IL-8. Our data demonstrate that platelets have the capacity to sense external signals differentially through a single type of pathogen recognition receptor and adjust the innate immune response appropriately for pathogens exhibiting different types of 'danger' signals.
authors.affiliation: Université de Lyon, F-42023, GIMAP, EA3064, Saint-Etienne, France.
authors.forename: Julien
authors.initials: J
authors.lastname: Berthet
authors.forename: Pauline
authors.initials: P
authors.lastname: Damien
authors.forename: Hind
authors.initials: H
authors.lastname: Hamzeh-Cognasse
authors.forename: Charles-Antoine
authors.initials: CA
authors.lastname: Arthaud
authors.forename: Marie-Ange
authors.initials: MA
authors.lastname: Eyraud
authors.forename: Fabrice
authors.initials: F
authors.lastname: Zéni
authors.forename: Bruno
authors.initials: B
authors.lastname: Pozzetto
authors.forename: Archibald
authors.initials: A
authors.lastname: McNicol
authors.forename: Olivier
authors.initials: O
authors.lastname: Garraud
authors.forename: Fabrice
authors.initials: F
authors.lastname: Cognasse
mesh_terms: D001792:Blood Platelets / Q000187:drug effects / Q000276:immunology*; D016207:Cytokines / Q000097:blood*; D004926:Escherichia coli / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate / Q000187:drug effects; D066298:In Vitro Techniques; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D007963:Leukocytes, Mononuclear / Q000276:immunology; D018950:Lipopolysaccharide Receptors / Q000097:blood; D008070:Lipopolysaccharides / Q000276:immunology* / Q000302:isolation & purification / Q000494:pharmacology; D019007:P-Selectin / Q000097:blood; D015539:Platelet Activation / Q000187:drug effects / Q000276:immunology; D020033:Protein Isoforms / Q000276:immunology / Q000302:isolation & purification / Q000494:pharmacology; D012475:Salmonella / Q000276:immunology; D015398:Signal Transduction / Q000276:immunology; D013045:Species Specificity; D060149:Tetraspanin 30 / Q000097:blood; D051197:Toll-Like Receptor 4 / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: C554586:CD63 protein, human; C508606:CXCL8 protein, human; D016207:Cytokines; C508600:IL6 protein, human; D015850:Interleukin-6; D016209:Interleukin-8; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D019007:P-Selectin; D020033:Protein Isoforms; C546937:SELP protein, human; C495345:TLR4 protein, human; D060149:Tetraspanin 30; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha