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.