IL-10 mediates monocyte hyporesponsiveness in septic shock

Introduction: Septic shock is associated with alterations in monocyte function, IL-10 has known immunosuppressive properties. We examined the role of IL-10 as a mediator of monocyte down regulation in septic shock. Methods: Blood mononuclear cells from healthy volunteers (n=10) were isolated and cultured. Culture plate adherent monocytes were incubated with either normal plasma (NP) or septic plasma (SP). Septic plasma was collected from septic shock patients within 24 hours of the diagnosis of sepsis. Following incubation with normal or septic plasma, LPS was added and the monocytes were incubated for 18 hours at 37°C (NPL or SPL). The supernatant was collected and analyzed for tumor necrosis factor (TNF-α), interleukin 1 (IL-1 β) and interleukin 10 (IL-10) by ELISA. In a parallel experiment antibody to IL-10 was added to the monocytes prior to adding the septic plasma and LPS (ASPL). Values are mean ± SEM,*p<0.05 vs. NPL Results: TNF-α ng/ml IL-10 pg/ml IL-1β pg/ml NP 2.62±2 36±25 152±152 NPL 36±9 359±113 4019±998 SP 1.8±.8 141±54 156±105 SPL 9±4*545±134 2035±466*ASPL 26±13 - 3429±943 Conclusion: Septic plasma significantly decreased monocyte release of TNF-α and IL-1 β in response to LPS stimulation. In contrast, the release of IL-10 was unchanged. The addition of antibody to IL-10 restored TNF-α and IL-1 βsecretion. The data suggest that IL-10 contributes to down regulation of monocyte function in septic shock.