Inhibitory effects of staphylococcal enterotoxin type B on human platelet adhesion in vitro

dc.creatorMorganti, RP
dc.creatorMarcondes, S
dc.creatorBaldasso, PA
dc.creatorMarangoni, S
dc.creatorDe Nucci, G
dc.creatorAntunes, E
dc.date2008
dc.date2014-11-18T06:54:32Z
dc.date2015-11-26T16:52:16Z
dc.date2014-11-18T06:54:32Z
dc.date2015-11-26T16:52:16Z
dc.date.accessioned2018-03-28T23:39:11Z
dc.date.available2018-03-28T23:39:11Z
dc.identifierPlatelets. Informa Healthcare, v. 19, n. 6, n. 432, n. 439, 2008.
dc.identifier0953-7104
dc.identifierWOS:000260120500006
dc.identifier10.1080/09537100802236035
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/80662
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/80662
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/80662
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1276234
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionSeptic shock was formerly recognized as a consequence of Gram-negative bacteraemia, but at present the incidence of Gram-positive sepsis seems to be more relevant, contributing for more than 50% of cases. Staphylococcal aureus can induce toxic shock in humans through the production of potent toxins termed Staphylococcal enterotoxins, from which Staphylococcal enterotoxin type B (SEB) is one of most studied. Platelets are reported to participate in pathogenesis of severe sepsis, but the exact role of platelets in this event is poorly investigated, particularly that caused by Gram-positive bacteria. Therefore, we have used the model of platelet adhesion to fibrinogen-coated plates to investigate the actions of SEB on human platelets. Ninety-six-well microtiter plates were coated with human fibrinogen (50 mu g/mL), and human washed platelet suspension (6 x 10(6) platelets) was added to each well. Adherent platelets were quantified through measurement of acid phosphatase activity. Staphylococcal enterotoxin B (0.0001-30 mu g/mL, incubated for 5 to 60 min) time- and dose-dependently inhibited platelet adhesion. This response was modified neither by the protein synthesis inhibitor puromycin (0.01 and 0.1 mM) nor by the superoxide scavengers superoxide dismutase (SOD, 100 units/mL) and polyethylene glycol-SOD (30 U/mL). The peroxide hydrogen (H(2)O(2)) scavenger catalase polyethylene glycol (1000 U/mL) significantly attenuated the platelet adhesion inhibition by SEB. The cAMP and cGMP levels were not changed by SEB (0.0001-30 mu g/mL, 60 min). Our findings suggest that H(2)O(2) at least partly contributes to the inhibitory responses of human platelet adhesion by SEB.
dc.description19
dc.description6
dc.description432
dc.description439
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.languageen
dc.publisherInforma Healthcare
dc.publisherLondon
dc.publisherInglaterra
dc.relationPlatelets
dc.relationPlatelets
dc.rightsfechado
dc.rightshttp://informahealthcare.com/userimages/ContentEditor/1255620309227/Copyright_And_Permissions.pdf
dc.sourceWeb of Science
dc.subjectStaphylococcal enterotoxins
dc.subjectcyclic nucleotides
dc.subjectperoxide hydrogen
dc.subjectplatelet adhesion
dc.subjectVasodilator-stimulated Phosphoprotein
dc.subjectAureus Lipoteichoic Acid
dc.subjectGlycoprotein-iib-iiia
dc.subjectNitric-oxide
dc.subjectHydrogen-peroxide
dc.subjectAntiplatelet Activity
dc.subjectEndothelial-cells
dc.subjectCalcium-entry
dc.subjectProtein
dc.subjectPhosphorylation
dc.titleInhibitory effects of staphylococcal enterotoxin type B on human platelet adhesion in vitro
dc.typeArtículos de revistas


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