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Infect Immun, June 1998, p. 2722-2727, Vol. 66, No. 6
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Effects of Granulocyte-Macrophage Colony-Stimulating Factor and Tumor Necrosis Factor Alpha on Trypanosoma cruzi Trypomastigotes

Elizabeth Olivares Fontt,1 Patrick De Baetselier,2 Carlo Heirman,3 Kris Thielemans,3 Ralph Lucas,2 and Bernard Vray1,*

Laboratoire d'Immunologie Expérimentale, Faculté de Médecine, Université Libre de Bruxelles,1 and Laboratory of Cellular Immunology, Flanders Interuniversity Institute for Biotechnology,2 and Laboratorium Fysiologie, Faculteit Geneeskunde,3 Vrije Universiteit Brussel, Brussels, Belgium

Received 19 August 1997/Returned for modification 9 October 1997/Accepted 19 March 1998

We have previously shown that the addition of exogenous granulocyte-macrophage colony-stimulating factor (GM-CSF) to nonactivated mouse peritoneal macrophages (MPM) limits Trypanosoma cruzi infections in vitro (E. Olivares Fontt and B. Vray, Parasite Immunol. 17:135-141, 1995). Lower levels of infection were correlated with a higher level of production of tumor necrosis factor alpha (TNF-alpha ) in the absence of nitric oxide (NO) release. These data suggested that GM-CSF and/or TNF-alpha might have a direct parasitocidal effect on T. cruzi trypomastigotes, independently of NO release. To address this question, T. cruzi trypomastigotes were treated with recombinant murine GM-CSF (rmGM-CSF), recombinant murine TNF-alpha (rmTNF-alpha ), or both cytokines in a cell-free system. Treatment with rmGM-CSF but not rmTNF-alpha caused morphological changes in the parasites, and most became spherical after 7 h of incubation. Both cytokines exerted a cytolytic activity on the trypomastigotes, yet the trypanolytic activity of rmTNF-alpha was more effective than that of rmGM-CSF. Viable rmGM-CSF- and rmTNF-alpha -treated parasites were less able to infect MPM than untreated parasites, and this reduction in infectivity was greatest for rmGM-CSF. Treatments with both cytokines resulted in more lysis and almost complete inhibition of infection. The direct parasitocidal activity of rmTNF-alpha was inhibited by carbohydrates and monoclonal antibodies specific for the lectin-like domain of TNF-alpha . Collectively, these results suggest that cytokines such as GM-CSF and TNF-alpha may directly control the level of T. cruzi trypomastigotes at least in vitro and so could determine the outcome of infection in vivo.

* Corresponding author. Mailing address: Laboratoire d'Immunologie Expérimentale (CP 615), Faculté de Médecine, Université Libre de Bruxelles, 808 route de Lennik, B-1070 Brussels, Belgium. Phone: 32-2-555.62.60. Fax: 32-2-555.63.60. E-mail: bvray{at}med.ulb.ac.be.

Infect Immun, June 1998, p. 2722-2727, Vol. 66, No. 6
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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