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Infection and Immunity, January 1999, p. 308-318, Vol. 67, No. 1
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Influence of Acute-Phase Parasite Load on Pathology, Parasitism, and Activation of the Immune System at the Late Chronic Phase of Chagas' Disease

Claudio R. F. Marinho,1 Maria Regina D'Império Lima,1 Marcos G. Grisotto,2 and José M. Alvarez1,*

Department of Immunology1 and Department of Parasitology,2 Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, SP, Brazil

Received 9 July 1998/Returned for modification 18 August 1998/Accepted 23 October 1998

To obtain low and high parasite loads in the acute phase of Chagas' disease, A/J mice were infected with 103 or 105 Trypanosoma cruzi trypomastigotes of the Y strain and treated on day 6 with benznidazol. One year later, chronically infected mice were screened for subpatent parasitemias, tissue pathology, and immune response. Mice infected with the high parasite inoculum showed higher levels of chronic parasitemias, heart and striated muscle inflammation, and activation of the immune system than did mice infected with the low inoculum. Concerning the activation of the immune system, the main findings for high-dose-infected mice were (i) increased numbers of splenocytes, with preferential expansion of CD8+ and B220- CD5- cells, many of them bearing a macrophage phenotype; (ii) higher frequencies of B (B220+), CD4+, and CD8+ large lymphocytes; (iii) a shift of CD4+ cells towards a CD45RBLow phenotype; (iv) increased frequencies of both CD45RBLow and CD45RBHigh large CD4+ cells; (v) augmented numbers of total immunoglobulin (Ig)-secreting cells, with predominance of IgG2a-producing cells; and (vi) increased production of gamma interferon and interleukin 4. In addition, these mice presented lower IgM and higher IgG2a and IgG1 parasite-specific serum antibody levels. Our results indicate that the parasite load at the acute phase of T. cruzi infection influences the activation of the immune system and development of Chagas' disease pathology at the late chronic phase of the disease.

* Corresponding author. Mailing address: Departamento de Imunologia, ICB, Av. Prof. Lineu Prestes, 1730, Universidade de São Paulo, São Paulo, SP, CEP-05508-900, Brazil. Phone: (55) (11) 818 7389. Fax: (55) (11) 818 7224. E-mail: jmamosig{at}biomed.icb2.usp.br.

Infection and Immunity, January 1999, p. 308-318, Vol. 67, No. 1
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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