Effect of interleukin-10 (IL-10) on experimental LPS-induced acute lung injury

The purpose of this study was to clarify the role of interleukin-10 (IL-10) during the development of acute lung injury induced by lipopolysaccharide (LPS) in a mouse model. When LPS was given to nude mice, the mortality rate was 100% at 48 h of the observation period. However, mortality was reduced to 30% when IL-10 was added concomitantly (P < 0.01). In the IL-10 group, a significant reduction of inflammatory change in lung tissue was observed. It was also found that peripheral neutrophils increased when IL-10 was added. When LPS and IL-10 were given concomitantly, the level of tumor necrosis factor (TNF)-α in both serum and bronchoalveolar lavage fluid (BALF) decreased significantly (P < 0.05). In-vitro observations were made concerning the influence of human neutrophils. Both neutrophil superoxide (O₂ ⁻) and elas-tase production were increased by TNF-α stimulation, while significant inhibition was seen with the concomitant dosing of IL-10 (P < 0.05). TNF-α stimulation increased the occurrence of adhesion molecules for neutrophil surface, lymphocyte function-associated antigen-1 (LFA-1), and macrophage antigen-1 (Mac-1). LPS stimulation greatly increased the occurrence of neutrophil surface 55-kDa TNF-receptor [TNF-R (p55)], when observation was made under laser microscopy. However, no significant occurrence was seen with IL-10 concomitant dosing. The above results suggested that IL-10 inhibited TNF-α production and neutrophil activity in LPS-induced acute lung injury, which led to a reduction of the lung tissue injury. Received: February 18, 1999 / Accepted: December 20, 1999