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Infection and Immunity, June 2004, p. 3129-3137, Vol. 72, No. 6
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.6.3129-3137.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Interleukin-10 Limits Local and Body Cavity Inflammation during Infection with Muscle-Stage Trichinella spiralis

Daniel P. Beiting,1* Susan K. Bliss,1 Donald H. Schlafer,2 Victoria L. Roberts,1 and Judith A. Appleton1

James A. Baker Institute for Animal Health,1 Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York2

Received 25 September 2003/ Returned for modification 21 November 2003/ Accepted 19 February 2004

The aim of this study was to characterize cellular responses to muscle-stage Trichinella spiralis. From its intracellular habitat in muscle, T. spiralis secretes potent glycoprotein antigens that elicit a strong systemic host immune response. Despite the magnitude and prolonged nature of this response, nurse cells are rarely destroyed by infiltrating cells. We tested the hypothesis that the anti-inflammatory cytokine interleukin-10 (IL-10) moderates cellular responses to muscle-stage parasites. Trichinella larvae colonize the diaphragm in large numbers, prompting us to evaluate regional responses in body cavities in addition to local responses in muscle. Mice deficient in IL-10 demonstrated an exaggerated inflammatory response around nurse cells and in the pleural cavity. The effect of IL-10 was most evident 20 days following muscle infection. The increased intensity of the response in IL-10-deficient mice did not affect parasite establishment or survival. Between 20 and 50 days postinfection, the inflammatory response was diminished in both wild-type and IL-10-deficient mice. Muscle infection also elicited an antibody response, characterized initially by mixed isotypes directed at somatic larval antigens and changing to an immunoglobulin G1-dominated response directed at tyvelose-bearing excreted or secreted antigens. We conclude that IL-10 limits local and regional inflammation during the early stages of muscle infection but that chronic inflammation is controlled by an IL-10-independent mechanism that is coincident with a Th2 response.

* Corresponding author. Mailing address: James A. Baker Institute for Animal Health, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853. Phone: (607) 256-5647. Fax: (607) 256-5608. E-mail: db225{at}cornell.edu.

Editor: J. F. Urban, Jr.

Infection and Immunity, June 2004, p. 3129-3137, Vol. 72, No. 6
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.6.3129-3137.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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