| First Author | Beiting DP | Year | 2004 |
| Journal | Infect Immun | Volume | 72 |
| Issue | 6 | Pages | 3129-37 |
| PubMed ID | 15155614 | Mgi Jnum | J:90250 |
| Mgi Id | MGI:3042754 | Doi | 10.1128/IAI.72.6.3129-3137.2004 |
| Citation | Beiting DP, et al. (2004) Interleukin-10 limits local and body cavity inflammation during infection with muscle-stage Trichinella spiralis. Infect Immun 72(6):3129-37 |
| abstractText | 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. |
