Interleukin 10 is not essential for survival or for modulating T-cell function after injury

Abstract

Background: Interleukin 10 (IL-10) is thought to be protective in injury and sepsis. However, we recently reported that IL-10 antagonism can be beneficial after burn injury. This study used IL-10–deficient (IL-10 [–/–]) mice to further define the role of IL-10 after injury. Methods: Wild-type (WT) C57BL/6 or IL-10 (–/–) mice were anesthetized, sham or burn injured, and immunized subcutaneously with a T-cell–dependent protein antigen. Ten days later antigen-specific serum antibody isotype formation was measured by enzyme-linked immunosorbent assay. In addition, antigen-stimulated splenic T-cell proliferation and cytokine production (interleukin 2, interferon gamma, and tumor necrosis factor-α) were measured. Results: Burn-injured IL-10 (–/–) mice survival (80%) was equivalent to that of burn-injured WT mice (74%). An injury-dependent loss of T-helper 1 (Th1)–type antibody isotype (IgG2a) formation occurred in both WT and IL-10 (–/–) mice. In vitro studies indicated that burn injury caused reduced antigen-stimulated splenic T-cell proliferation and Th1-type (interleukin 2 and interferon gamma) cytokine production in WT and IL-10 (–/–) mice, whereas burn-injured IL-10 (–/–) mice produced high levels of antigen-stimulated tumor necrosis factor-α. Conclusions: IL-10 is not essential for survival after burn injury or for several injury-induced changes in adaptive immune function, including Th1-type antibody isotype formation, T-cell proliferation, and Th1-type cytokine production. (Surgery 1999;126:456-62.)