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Infection and Immunity, March 2001, p. 1454-1462, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1454-1462.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Interleukin-12 Promotes Pathologic Liver Changes and Death in Mice Coinfected with Schistosoma mansoni and Toxoplasma gondii

Maria Ilma Araujo,1,2 Susan K. Bliss,1 Yasuhiro Suzuki,3 Ana Alcaraz,4 Eric Y. Denkers,1,* and Edward J. Pearce1

Department of Microbiology and Immunology1 and New York State Diagnostic Laboratory,4 College of Veterinary Medicine, Cornell University, Ithaca, New York 14853; Servico de Imunologia, Hospital Universitario Prof. Edgard Santos, Universidade Federal da Bahia, Bahia, Brazil2; and Department of Immunology and Infectious Diseases, Research Institute, Palo Alto Medical Foundation, and Division of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford University School of Medicine, Palo Alto, California 493013

Received 22 August 2000/Returned for modification 11 October 2000/Accepted 30 November 2000

We previously demonstrated that mice concurrently infected with Schistosoma mansoni and Toxoplasma gondii undergo accelerated mortality which is preceded by severe liver damage. Abnormally high levels of serum tumor necrosis factor alpha (TNF-alpha ) in the dually infected mice suggested a role for this and related proinflammatory mediators in the pathologic alterations. In order to evaluate the factors involved in increased inflammatory-mediator production and mortality, interleukin-12-/- (IL-12-/-) mice were coinfected with S. mansoni and T. gondii, and survival and immune responses were monitored. These IL-12-/- mice displayed decreased liver damage and prolonged time to death relative to wild-type animals also coinfected with these parasites. Relative to the response of cells from the coinfected wild-type animals, levels of TNF-alpha , gamma interferon, and NO produced by splenocytes from coinfected IL-12-/- mice were reduced, and levels of IL-5 and IL-10 were increased, with the net result that the immune response of the dually infected IL-12-/- mice was similar to that of the wild-type mice infected with S. mansoni alone. While dually infected wild-type animals succumb in the absence of overt parasitemia, the delayed death in the absence of IL-12 is associated with relatively uncontrolled T. gondii replication. These data support the view that S. mansoni-infected mice are acutely sensitive to infection with T. gondii as a result of their increased hepatic sensitivity to high levels of proinflammatory cytokines; IL-12 and TNF-alpha are implicated in this process.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853-6401. Phone: (607) 253-4022. Fax: (607) 253-3384. E-mail: eyd1{at}cornell.edu.

Infection and Immunity, March 2001, p. 1454-1462, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1454-1462.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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