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Infection and Immunity, November 1998, p. 5167-5174, Vol. 66, No. 11
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Altered Immune Responses in Mice with Concomitant Schistosoma mansoni and Plasmodium chabaudi Infections

Helena Helmby,* Marika Kullberg,dagger and Marita Troye-Blomberg

Department of Immunology, Stockholm University, Stockholm, Sweden

Received 19 May 1998/Returned for modification 29 July 1998/Accepted 13 August 1998

Mixed parasitic infections are common in many parts of the world. However, little is known about how concurrent infections affect the immunity to and/or pathogenesis of each other. Protection and elimination of blood-stage Plasmodium chabaudi chabaudi AS in resistant mice are characterized by a sequential activation of CD4+ Th1 and Th2 cells. The patent egg-laying stage of the murine model of Schistosoma mansoni is associated with a strong Th2 response to both Schistosoma and unrelated antigens. In this study, we investigated how infection of mice with S. mansoni would affect the immune response to and pathogenesis of a P. chabaudi infection. C57BL/6 mice infected with S. mansoni for 8 weeks were infected with blood-stage P. chabaudi. Malaria parasitemias were significantly higher in these mice than in mice infected with P. chabaudi only. In doubly infected mice, both spleen cell proliferative and Th2 responses to S. mansoni soluble egg antigen (SEA) or anti-CD3 were suppressed up to 1 month after the malaria infection. Findings for SEA-specific immunoglobulin M (IgM) and IgG serum antibody levels were similar. No significant effects were seen on P. chabaudi-induced gamma interferon responses. However, tumor necrosis factor alpha (TNF-alpha ) production was significantly lower in double-infected mice. Thus, a defect in TNF-alpha production might contribute to the increased malaria parasitemias seen in S. mansoni-P. chabaudi-infected mice. Taken together, our data show that schistosoma and malaria infections profoundly affect each other, findings which might have implications for the development of vaccines.

* Corresponding author. Mailing address: Dept. of Immunology, Stockholm University, Biology Building F5, S-106 91 Stockholm, Sweden. Phone: 46 8 16 41 70. Fax: 46 8 15 73 56. E-mail: helena{at}imm2.su.se.

dagger Present address: Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Md.

Infection and Immunity, November 1998, p. 5167-5174, Vol. 66, No. 11
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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