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Infection and Immunity, September 2003, p. 4996-5004, Vol. 71, No. 9
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.9.4996-5004.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Schistosomiasis Decreases Central Nervous System Inflammation and Alters the Progression of Experimental Autoimmune Encephalomyelitis

Anne Camille La Flamme,1* Kate Ruddenklau,2 and B. Thomas Bäckström2

School of Biological Sciences, Victoria University of Wellington,1 Malaghan Institute of Medical Research and Department of Pathology and Molecular Medicine, Wellington School of Medicine, Wellington, New Zealand2

Received 24 February 2003/ Returned for modification 14 April 2003/ Accepted 18 June 2003

A preestablished infection with the parasitic helminth, Schistosoma mansoni, significantly reduced the incidence and delayed the onset of experimental autoimmune encephalomyelitis (EAE) in C57BL/6J mice immunized with myelin oligodendrocyte glycoprotein (MOG)35-55 peptide. The altered disease progression was not solely due to the induction of a strong Th2 response, since intraperitoneal injection of schistosome eggs did not affect disease development. MOG-specific gamma interferon (IFN-{gamma}), nitric oxide, and tumor necrosis factor alpha production by splenocytes was significantly reduced in schistosome-infected mice compared to uninfected mice. However, similar levels of interleukin-10 (IL-10) were produced in an antigen-specific manner, suggesting that the induction of antigen-specific responses was not inhibited. Analysis of in vivo cytokine production by real-time PCR indicated that IL-12p40, but not IFN-{gamma}, transcript levels were dramatically reduced in the spinal cords of schistosome-infected, MOG-immunized mice. Furthermore, analysis of the cellular composition of the spinal cords and brains revealed that a preestablished infection with S. mansoni decreased central nervous system (CNS) inflammation, particularly of macrophages and CD4 T cells. These results suggest that schistosomiasis may negatively regulate the onset of EAE by downregulating the production of proinflammatory cytokines and altering CNS inflammation.

* Corresponding author. Mailing address: School of Biological Sciences, Victoria University of Wellington, P.O. Box 600, Wellington, New Zealand. Phone: 64-4-463-6093. Fax: 64-4-463-5331. E-mail: anne.laflamme{at}vuw.ac.nz.

Editor: J. M. Mansfield

Infection and Immunity, September 2003, p. 4996-5004, Vol. 71, No. 9
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.9.4996-5004.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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