Interleukin-10 protects against IgG immune complex-induced lung injury through suppression of NF-κB

Administration of exogenous IL-10 reduces the inflammatory lung injury induced by IgG immune complex deposition. These protective effects are mediated through reduced production of pulmonary TNF-α and decreased expression of the adhesion molecule ICAM-1. In vitro studies have demonstrated that both TNF-α and ICAM-1 gene expression are under the control of the nuclear transcription factor NF-κB. The objective of the current study was to determine whether exogenously administered IL-10 can regulate NF-κB activity in vivo. Using electrophoretic mobility shift assays, we found that the nuclear localization of NF-κB in lung tissue was increased 0.5, 2 and 3 hours after the induction of lung injury in rats. The administration of IL-10 attenuated the nuclear localization of NF-κB at all three time points. Similar results were obtained from alveolar macrophages obtained by bronchoalveolar lavage 30 minutes after the induction of injury. The results demonstrate that IL-10 suppresses NFκB activation in vivo. These findings suggest that IL-10 protects against lung inflammatory injury by reducing gene expression under the control of NF-κB.