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 al ter the susceptibility to subsequent infections by other pathogens, particu larly intracellular parasites. We therefore explored whether a persistent i nfection, caused by Taenia crassiceps cysticerci, in BALB/c mice could affe ct 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 ti me-course evolution of the initial infection. Coinfection with the protozoa n in the early stages of the helminth infection, induced a delay on the ons et of parasitaemia, early specific production of IFN-gamma and high specifi c production of IL-4. A significant increase in susceptibility to T. cruzi was observed only when mice were coinfected in late stages when the helmint h 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 hel minth infections could potentially have a significant influence over the im mune response and hence susceptibility to other pathogens.