Some characteristics of hyperreactivity to bacterial lipopolysaccharide induced in mice by Trypanosoma cruzi infection

Abstract

Mice infected with T. cruzi strain, acquire a high level of susceptibility to the effects of bacterial gram-negative LPS. The LD50 of adult female SW mice to LPS from S. typhosa, decreases from 450 to 2,5 mcg 10-12 days after T. cruzi infection. This hyperreactivity to LPS induced by T. cruzi presents all the characteristics of that found in infection caused by many other agents. During the acaute phase of experimental infection with T. cruzi Y strain, mice generally die with a hypovolemic shock very similar to that induced in uninfected animals injected with an adequate dose of bacterial endotoxin. There is evidence for and against the hypothesis that LPS absorbed from the instestinal tract may be involved in the mechanism of death of mice during the acute phase of T. cruzi infection.Camundongos infectados com a cepa Y do T. cruzi adquirem elevado grau de reatividade ao LPS de S. typhosa. A LD50 de camundongos SW, adultos, fêmeas, com peso em torno de 20g, decresce de 450 para 2,5mcg ao fim de 10-12 dias de infecção. Esta hiperatividade ao LPS induzida pelo T. cruzi apresenta todas as características daquela encontrada nas infecções causadas por muitos outros agentes. Durante a fase aguda da infecção experimental com T. cruzi, cepa Y, os camundongos geralmente morrem com choque hipovolêmico muito semelhante ao ocasionado por dose adequada de endotoxina bacteriana. Há evidências a favor e contra a hipótese de que os LPS liberados do trato instestinal setejam envolvidos no mecanismo de morte do camundongo durante a fase aguda da infecção pela cepa Y do T. cruzi.