The role of interleukin-10 in systemic inflammatory response syndrome with sepsis

This study was performed to demonstrate the role of interleukin (IL)-10, especially in systemic inflammatory response syndrome (SIRS) patients. In clinical observations, levels of serum tumor necrosis factor-α (TNF) and IL-10 increased in SIRS patients (TNF, n=43; IL-10, n=33), and they increased more in the patients with organ failure (n=22) than in patients without organ failure (n=24), (P<0.01). In mice, serum TNF and IL-10 began to increase at 1 hour after injection with 4mg/kg of lipopolysaccharide (LPS) and reached a maximum at 2 hours. However, the serum level of TNF decreased to an undetectable level at 6 hours, while a significant amount of IL-10 remained in serum. The TNF elevation induced by LPS injection was inhibited by pretreatment with 200 ng of IL-10 (P<0.1 in serum,P<0.05 in bronchoalveolar lavage fluid). Neutrophil reduction induced by LPS injection was also inhibited by pretreatment with 1 μg of IL-10. On human neutrophils the expression of adhesion molecules LFA-1 and MAC-1 that resulted from in vitro incubation with TNF were suppressed by the addition of IL-10 supplement. The expression of TNF receptors on the surface of human neutrophils as a result of LPS loading was also suppressed by IL-10 supplement. IL-10 seems have a protective function in the progress to organ failure in SIRS patients with sepsis. IL-10 suppresses TNF production and inhibits the expression of adhesion molecules and TNF receptors on neutrophils.