Monocyte subsets along with their inflammatory cytokines in septic lung injury: anti-inflammatory effect of sulfotransferase homolog 2 receptors blockade

Monocytes which are phenotypically and functionally heterogeneous contribute to septic organ damage by producing various inflammatory cytokines. The interleukin (IL)-33/sulfotransferase homolog 2 (ST2) is closely related to sepsis. The regulation effect of ST2 receptors on monocytes is not fully understood. This study aims to detect changes of monocyte subsets during septic lung injury and elucidate the effect of ST2 receptors on monocytes. Dynamic changes of monocyte subsets from patients with septic lung injury and mice post cecal ligation and puncture (CLP) were monitored. ST2 receptors on mice monocytes and concentrations of IL-33, IL-1β, IL-12 and IL-27 from peripheral blood or culture supernatant were detected. The results showed a novel CD14 low CD16 − subset monocytes from peripheral blood of sepsis patients dramatically increased. Mice blood levels of IL-33, IL-1β, IL-12 and IL-27 were much higher in the CLP 24h group. There was expression of ST2 receptors on mice monocytes. Monocytes’ production of pro-inflammatory cytokines IL-1β and IL-12 induced by lipopolysaccharide (LPS) and IL-33 reduced when the ST2 receptors blockade. Changes of monocyte subsets with expression of ST2 receptors might play a role during septic lung injury by modulating inflammatory cytokines secretion, which might be novel targets for lung protection during sepsis.