Trypanosoma cruzi does not induce apoptosis in murine fibroblasts

The intracellular cycle of Trypanosoma cruzi in mammalian host cells involv es the differentiation of dividing amastigote forms into flagellated trypom astigote forms. The mechanism(s) regulating the growth and differentiation of the intracellular parasites is (are) not known. The number of parasites in infected cells can be several hundred and may be enough to induce apopto sis, a suicide-like death programme, generating products (e.g. nuclear prot eins) that could function as signals to initiate the differentiation of ama stigotes into trypomastigotes. Murine fibroblasts infected with T. cruzi we re examined during a 5-day course of infection for evidence of apoptosis. H owever, characteristics of apoptosis, including degeneration of nuclear str ucture, condensation of chromatin, loss of plasma membrane integrity, or th e cleavage of DNA into nucleosomal fragments, were not observed. Therefore, it is unlikely that products resulting from host cell apoptosis function t o induce parasite differentiation. The possibility that T. cruzi might inhi bit host cell apoptosis bq increasing intracellular levels of Bcl-2, an end ogenous inhibitor of apoptosis, was then investigated. Analysis of infected cells by flow cytometry did not demonstrate a significant amount of intrac ellular Bcl-2. This suggests that if the parasite is inhibiting host cell a poptosis, it is by a method that does not involve increasing levels of Bcl- 2.