Trypanosoma Cruzi sensitizes mice to fulminant seb-induced Shock: Overrelease of Iinflammatory cytokines and independence of Chagas’ Disease or TCR Vb-Usage

dc.creatorPaiva Neto, Claúdia
dc.creatorPyrrho, Alexandre dos Santos
dc.creatorVieira, Joseli Lannes
dc.creatorVacchio, Melanie
dc.creatorSoares, Milena Botelho Pereira
dc.creatorGattass, Cerli Rocha
dc.date2016-09-27T13:21:11Z
dc.date2016-09-27T13:21:11Z
dc.date2003
dc.date.accessioned2023-09-26T20:49:05Z
dc.date.available2023-09-26T20:49:05Z
dc.identifierPAIVA NETO, C. et al. Trypanosoma Cruzi sensitizes mice to fulminant seb-induced Shock: Overrelease of Iinflammatory cytokines and independence of Chagas’ Disease or TCR Vb-Usage. Shock, v. 19, n. 2, p. 163–168, 2003.
dc.identifier1073-2322
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/15958
dc.identifier10.1097/01.SHK.0000054747.80210.e9
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8864419
dc.descriptionPrograma de Apoio a Núcleos de Excelência Conselho Nacional de Pesquisas. Fundação de Amparo a Pesquisa de Estado do Rio de Janeiro. World Health Organization
dc.descriptionTrypanosoma cruzi–infected mice display increased susceptibility to shock induced by injection of lipopolysaccharide (LPS), anti-CD3, or resulting from interleukin (IL)-10-defective response to the parasite itself, but the basis of such susceptibility remains unknown. Herein, we tested the susceptibility of mice inoculated with virulent and avirulent T. cruzi to staphylococcal enterotoxins (SE), potent inducers of inflammatory cytokine secretion. Mice infected with T. cruzi CL-strain or inoculated with the avirulent clone CL-14, a clone that does not induce disease or polyclonal lymphocyte activation, succumb suddenly to low doses of staphylococcal enterotoxin B (SEB), but not to staphylococcal enterotoxin A (SEA). High plasma levels of TNF, IFN-g, and liver transaminases alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were found in these mice, indicating lethal toxic shock. Sensitization to shock required inoculation of live avirulent trypomastigotes and a time interval before challenge with SEB. We found no prior skewing of T cell receptor (TCR) Vb-repertoire in CL-14-inoculated mice that could be responsible for sensitization. Splenocytes from CL-14-inoculated mice proliferated more under anti-Vb8 than anti-TCRb stimulation when compared with normal mice, but were suppressed to SEB stimulation. Both SEB and anti-Vb8 antibodies stimulated splenocytes from T. cruzi-inoculated mice to secrete higher levels of inflammatory cytokines than normal controls. Taken together, our results show that T. cruzi inoculation can sensitize mice to lethal SEB-induced shock even in the absence of tissue damage, polyclonal lymphocyte activation, or previously increased levels of inflammatory cytokines, and they suggest that altered reactivity of Vb8 lymphocytes may be involved in the phenomenon
dc.formatapplication/pdf
dc.languageeng
dc.publisherLippincott, Williams & Wilkins
dc.rightsopen access
dc.subjectRepertório
dc.subjectClone CL-14
dc.subjectCepa CL
dc.subjectEnterotoxina B de estafilococos
dc.subjectSepsia
dc.subjectLinfócitos T
dc.subjectTNF-a
dc.subjectIFN-g
dc.subjectRepertoire
dc.subjectClone CL-14
dc.subjectCL strain
dc.subjectStaphylococcal enterotoxin B
dc.subjectSepsis
dc.subjectT lymphocyte
dc.subjectTNF-a
dc.subjectIFN-g
dc.titleTrypanosoma Cruzi sensitizes mice to fulminant seb-induced Shock: Overrelease of Iinflammatory cytokines and independence of Chagas’ Disease or TCR Vb-Usage
dc.typeArticle


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