Parasitology



Trypanosoma cruzi does not induce apoptosis in murine fibroblasts


R. K. CLARK a1 and R. E. KUHN a1c1
a1 Department of Biology, Wake Forest University, P.O. Box 7325, Winston-Salem, NC 27109, USA

Abstract

The intracellular cycle of Trypanosoma cruzi in mammalian host cells involves the differentiation of dividing amastigote forms into flagellated trypomastigote 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 apoptosis, a suicide-like death programme, generating products (e.g. nuclear proteins) that could function as signals to initiate the differentiation of amastigotes into trypomastigotes. Murine fibroblasts infected with T. cruzi were examined during a 5-day course of infection for evidence of apoptosis. However, characteristics of apoptosis, including degeneration of nuclear structure, condensation of chromatin, loss of plasma membrane integrity, or the cleavage of DNA into nucleosomal fragments, were not observed. Therefore, it is unlikely that products resulting from host cell apoptosis function to induce parasite differentiation. The possibility that T. cruzi might inhibit host cell apoptosis by increasing intracellular levels of Bcl-2, an endogenous inhibitor of apoptosis, was then investigated. Analysis of infected cells by flow cytometry did not demonstrate a significant amount of intracellular Bcl-2. This suggests that if the parasite is inhibiting host cell apoptosis, it is by a method that does not involve increasing levels of Bcl-2.

(Received April 29 1998)
(Revised July 28 1998)
(Accepted July 29 1998)


Key Words: Trypanosoma cruzi; apoptosis; cell death; murine fibroblasts.

Correspondence:
c1 Corresponding author: P.O. Box 7325, Department of Biology, Wake Forest University, Winston-Salem, NC 27109, USA. Tel +336 758 5022. Fax: +336 768 6008. E-mail: kuhnray@wfu.edu


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