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Antimicrobial Agents and Chemotherapy, December 2002, p. 3790-3796, Vol. 46, No. 12
0066-4804/02/$04.00+0     DOI: 10.1128/AAC.46.12.3790-3796.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Benznidazole Treatment following Acute Trypanosoma cruzi Infection Triggers CD8+ T-Cell Expansion and Promotes Resistance to Reinfection

Bianca Perdigão Olivieri, Vinícius Cotta-de-Almeida,{dagger} and Tania Araújo-Jorge*

Laboratory of Cell Biology, Department of Ultrastructure and Cell Biology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil

Received 25 March 2002/ Returned for modification 2 July 2002/ Accepted 27 August 2002

Many studies have shed light on the mechanisms underlying both immunoprotection and immune dysregulation arising after Trypanosoma cruzi infection. However, little is known about the impact of benznidazole (N-benzyl-2-nitroimidazole acetamide), the drug available for clinical treatment of the infection, on the immune system in the infected host. In the present study we investigated the effect of benznidazole therapy on the lymphoid compartment during the course of experimental T. cruzi infection. Although amelioration of a variety of clinical and parasitological signs was observed in treated mice, amelioration of splenocyte expansion was not detected. Interestingly, this sustained splenomegaly observed in benznidazole-treated mice showed a preferential expansion of CD8+ T lymphocytes. Moreover, although benznidazole treatment blocked the expansion of recently activated CD4+ and CD8+ T cells seen in infected hosts, benznidazole treatment led to a selective expansion of effector and memory CD8+ T lymphocytes in association with a lower rate of apoptosis. In addition, the surviving treated animals were protected from reinfection. Together, these data suggest that, in addition to its well-known direct role in blocking parasite replication in vivo, benznidazole appears to directly affect immune regulation in T. cruzi-infected hosts.

* Corresponding author. Mailing address: Laboratory of Cell Biology, Department of Ultrastructure and Cell Biology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Ave. Brasil 4365, Rio de Janeiro 21045-900, Brazil. Phone: (55) 21-2598-4330. Fax: (55) 21-2260-4434. E-mail: taniaaj{at}ioc.fiocruz.br.

{dagger} Present address: Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Mass.

Antimicrobial Agents and Chemotherapy, December 2002, p. 3790-3796, Vol. 46, No. 12
0066-4804/02/$04.00+0     DOI: 10.1128/AAC.46.12.3790-3796.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Ferraz, M. L., Gazzinelli, R. T., Alves, R. O., Urbina, J. A., Romanha, A. J. (2009). Absence of CD4+ T Lymphocytes, CD8+ T Lymphocytes, or B Lymphocytes Has Different Effects on the Efficacy of Posaconazole and Benznidazole in Treatment of Experimental Acute Trypanosoma cruzi Infection. Antimicrob. Agents Chemother. 53: 174-179 [Abstract] [Full Text]  
  • Hyland, K. V., Leon, J. S., Daniels, M. D., Giafis, N., Woods, L. M., Bahk, T. J., Wang, K., Engman, D. M. (2007). Modulation of Autoimmunity by Treatment of an Infectious Disease. Infect. Immun. 75: 3641-3650 [Abstract] [Full Text]  
  • Olivieri, B. P., Farias-De-Oliveira, D. A., Araujo-Jorge, T. C., Cotta-de-Almeida, V. (2005). Benznidazole Therapy in Trypanosoma cruzi-Infected Mice Blocks Thymic Involution and Apoptosis of CD4+CD8+ Double-Positive Thymocytes. Antimicrob. Agents Chemother. 49: 1981-1987 [Abstract] [Full Text]  


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