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Infection and Immunity, December 1999, p. 6565-6571, Vol. 67, No. 12
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Cytokine Control of the Granulomatous Response in Schistosoma mansoni-Infected Baboons: Role of Exposure and Treatment

Paul W. Mola,1,2 Idle O. Farah,1 Thomas M. Kariuki,1 Mramba Nyindo,1 Ronald E. Blanton,2 and Christopher L. King2,*

Division of Infectious Diseases, Institute of Primate Research, National Museums of Kenya, Karen, Nairobi, Kenya,1 and Division of Geographic Medicine, School of Medicine, Case Western Reserve University, Cleveland, Ohio2

Received 8 July 1999/Returned for modification 25 August 1999/Accepted 22 September 1999

Variations in exposure and treatment may contribute to heterogeneity in immunity and granuloma-induced pathology in human schistosomiasis. To examine this hypothesis, olive baboons were either repeatedly infected with Schistosoma mansoni cercariae or received an equivalent dose in a single infection. They were then cured with praziquantel and reinfected with a single exposure. Serial liver biopsies were obtained throughout the course of the experiment, and cytokine responses by peripheral blood mononuclear cells were measured every 2 to 3 weeks. Reinfection after treatment resulted in a twofold-smaller granuloma size at 6 and 9 weeks after infection compared to the size for the same period after primary infection (P < 0.001) but had no effect at 16 or 19 weeks postinfection. The pattern of exposure did not influence granuloma size. During primary infection schistosome-soluble egg antigen (SEA)-induced cytokine production correlated with granulomatous inflammation. Cytokine levels peaked during the acute infection, declined with chronic infection, and became undetectable after treatment. Reinfection after treatment stimulated a two- to three-fold increase in SEA-specific interleukin-4 (IL-4), IL-5, IL-10, IL-2, and transforming growth factor beta  (TGF-beta ) production and a marked rise in SEA-specific immunoglobulin E (IgE) and IgG regardless of the type of exposure. Cytokine production was significantly greater in repeatedly exposed animals (P < 0.001). SEA-induced gamma interferon production, however, did not increase with reinfection after treatment. SEA-induced TGF-beta was the only cytokine that remained elevated as the infection become chronic and correlated with diminished hepatic granuloma size, implying its participation in down-modulation. These studies demonstrate that baboons partially retain their ability to down-modulate the granulomatous response after treatment.

* Corresponding author. Mailing address: Division of Geographic Medicine, School of Medicine, Case Western Reserve University, 2109 Adelbert Rd., Cleveland, OH 44106-4983. Phone: (216) 368-4817. Fax: (216) 368-4825. E-mail: cxk21{at}po.cwru.edu.

Infection and Immunity, December 1999, p. 6565-6571, Vol. 67, No. 12
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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