Previous Article | Next Article 
Infect Immun, June 1998, p. 2722-2727, Vol. 66, No. 6
Laboratoire d'Immunologie
Expérimentale,
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-
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
) in the absence of nitric oxide
(NO) release. These data suggested that GM-CSF and/or
TNF- 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- (rmTNF-), or both cytokines in a cell-free
system. Treatment with rmGM-CSF but not rmTNF- 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- was more effective than that of
rmGM-CSF. Viable rmGM-CSF- and rmTNF--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- was inhibited
by carbohydrates and monoclonal antibodies specific for the lectin-like domain of TNF-. Collectively, these results suggest that cytokines such as GM-CSF and TNF- 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.
This article has been cited by other articles:
-
Chamekh, M., Vercruysse, V., Habib, M., Lorent, M., Goldman, M., Allaoui, A., Vray, B.
(2005). Transfection of Trypanosoma cruzi with Host CD40 Ligand Results in Improved Control of Parasite Infection. Infect. Immun.
73: 6552-6561
[Abstract] [Full Text] -
Cummings, K. L., Tarleton, R. L.
(2004). Inducible Nitric Oxide Synthase Is Not Essential for Control of Trypanosoma cruzi Infection in Mice. Infect. Immun.
72: 4081-4089
[Abstract] [Full Text] -
Dumas, C., Muyombwe, A., Roy, G., Matte, C., Ouellette, M., Olivier, M., Papadopoulou, B.
(2003). Recombinant Leishmania major Secreting Biologically Active Granulocyte-Macrophage Colony-Stimulating Factor Survives Poorly in Macrophages In Vitro and Delays Disease Development in Mice. Infect. Immun.
71: 6499-6509
[Abstract] [Full Text] -
Deepe, G. S. Jr., Gibbons, R.
(2000). Recombinant Murine Granulocyte-Macrophage Colony-Stimulating Factor Modulates the Course of Pulmonary Histoplasmosis in Immunocompetent and Immunodeficient Mice. Antimicrob. Agents Chemother.
44: 3328-3336
[Abstract] [Full Text]
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»