Susceptibility to Trypanosoma cruzi is modified by a previous non-related infection.
Helminth infections are frequently massive, chronic and strong inductors of Th2-type cytokines. This implies that infection by such parasites could alter the susceptibility to subsequent infections by other pathogens, particularly intracellular parasites. We therefore explored whether a persistent infection, caused by Taenia crassiceps cysticerci, in BALB/c mice could affect susceptibility to a later infection by Trypanosoma cruzi. We found that the presence of the cysticerci indeed modified the immune response and the susceptibility to T. cruzi, and that these modifications depended on the time-course evolution of the initial infection. Coinfection with the protozoan in the early stages of the helminth infection, induced a delay on the onset of parasitaemia, early specific production of IFN-gamma and high specific production of IL-4. A significant increase in susceptibility to T. cruzi was observed only when mice were coinfected in late stages when the helminth load is greater and a Th2 type response against it is predominant. The in vitro specific response to T. cruzi antigens was then characterized by low levels of both IFN-gamma and IL-4. These findings suggest that chronic helminth infections could potentially have a significant influence over the immune response and hence susceptibility to other pathogens.
D000818:Animals; D000918:Antibody Specificity; D000947:Antigens, Helminth / Q000097:blood; D014355:Chagas Disease / Q000150:complications / Q000276:immunology*; D003208:Concanavalin A / Q000494:pharmacology; D003551:Cysticercosis / Q000150:complications / Q000276:immunology*; D016207:Cytokines / Q000378:metabolism; D005260:Female; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000166:cytology / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D018512:Parasitemia; D013154:Spleen / Q000166:cytology / Q000276:immunology