Article
Trypanosoma Cruzi sensitizes mice to fulminant seb-induced Shock: Overrelease of Iinflammatory cytokines and independence of Chagas’ Disease or TCR Vb-Usage
Registro en:
PAIVA 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.
1073-2322
10.1097/01.SHK.0000054747.80210.e9
Autor
Paiva Neto, Claúdia
Pyrrho, Alexandre dos Santos
Vieira, Joseli Lannes
Vacchio, Melanie
Soares, Milena Botelho Pereira
Gattass, Cerli Rocha
Resumen
Programa de Apoio a Núcleos de Excelência Conselho Nacional de Pesquisas. Fundação de Amparo a Pesquisa de Estado do Rio de Janeiro. World Health Organization Trypanosoma 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