Regulatory effects of interleukin-11 during acute lung inflammatory injury

The role of interleukin-11 (IL-11) was evaluated in the IgG immune complex model of acute lung injury in rats, IL-11 mRNA and protein were both up-regulated during the course of this inflammatory response. Exogenously administered IL-11 substantially reduced, in a dose-dependent manner, the intrapulmonary accumulation of neutrophils and the lung vascular leak of albumin, These in vitro anti-inflammatory effects of IL-11 were associated with reduced NF-kappa B activation in lung, reduced levels of tumor necrosis factor alpha (TNF-alpha) in bronchoalveolar lavage (BAL) fluids, and diminished up-regulation of lung vascular ICAM-1. It is interesting that IL-11 did not affect BAL fluid content of the CXC chemokines, macrophage inflammatory protein-2 (MIP-2) and cytokine-inducible neutrophil chemoattractant (CINC); the presence of IL-11 did not affect these chemokines, However, BAL content of C5a was reduced by IL-11. These data indicate that IL-11 is a regulatory cytokine in the lung and that, Like other members of this family, its anti-inflammatory properties appear to be linked to its suppression of NF-kappa B activation, diminished production of TNF-alpha, and reduced up-regulation of lung vascular ICAM-1.