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Infection and Immunity, April 2005, p. 2515-2523, Vol. 73, No. 4
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.4.2515-2523.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Potential Role of the Chemokine Macrophage Inflammatory Protein 1{alpha} in Human and Experimental Schistosomiasis

Adriano L. S. Souza,1 Ester Roffê,1 Vanessa Pinho,1 Danielle G. Souza,1 Adriana F. Silva,2 Remo C. Russo,1 Rodrigo Guabiraba,1 Cíntia A. J. Pereira,2 Flávia M. Carvalho,1 Michele M. Barsante,1 Rodrigo Correa-Oliveira,3 Lúcia A. O. Fraga,4 Deborah Negrão-Correa,2 and Mauro M. Teixeira1*

Laboratório de Imunofarmacologia, Departamento de Bioqu¡mica e Imunologia,1 Grupo Interdisciplinar de Estudos em Esquistossomose, Departamento de Parasitologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, and,2 Laboratório de Imunologia Celular, Centro de Pesquisa René Rachou, Fundação Oswaldo Cruz Belo Horizonte,3 Laboratório de Imunologia, Universidade do Vale do Rio Doce, Montes Claros, Brazil4

Received 7 July 2004/ Returned for modification 19 August 2004/ Accepted 11 November 2004

In human schistosomiasis, the concentrations of the chemokine macrophage inflammatory protein 1{alpha} (MIP-1{alpha}/CCL3) is greater in the plasma of patients with clinical hepatosplenic disease. The objective of the present study was to confirm the ability of CCL3 to detect severe disease in patients classified by ultrasonography (US) and to evaluate the potential role of CCL3 in Schistosoma mansoni-infected mice. CCL3 was measured by enzyme-linked immunosorbent assay in the plasma of S. mansoni-infected patients. CCL3-deficient mice were infected with 25 cercariae, and various inflammatory and infectious indices were evaluated. The concentration of CCL3 was higher in the plasma of S. mansoni-infected than noninfected patients. Moreover, CCL3 was greater in those with US-defined hepatosplenic than with the intestinal form of the disease. In CCL3-deficient mice, the size of the granuloma and the liver eosinophil peroxidase activity and collagen content were diminished compared to wild-type mice. In CCL3-deficient mice, the worm burden after 14 weeks of infection, but not after 9 weeks, was consistently smaller. The in vitro response of mesenteric lymph node cells to antigen stimulation was characterized by lower levels of interleukin-4 (IL-4) and IL-10. CCL3 is a marker of disease severity in infected humans, and experimental studies in mice suggest that CCL3 may be a causative factor in the development of severe schistosomiasis.

* Corresponding author. Mailing address: Laboratório de Imunofarmacologia, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. Phone: 55-31-3499-2651. Fax: 55-31-3499-2651. E-mail: mmtex{at}icb.ufmg.br.

Editor: J. F. Urban, Jr.

Infection and Immunity, April 2005, p. 2515-2523, Vol. 73, No. 4
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.4.2515-2523.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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