Naturally existing CD11c(low)CD45RB(high) dendritic cells protect mice from acute severe inflammatory response induced by thermal injury.

Despite a good understanding of the process that initiates and promotes host inflammation induced by acute injury, little is known about the host immune cells responsible for the inhibition of inflammatory response to thermal injury. The aim of this study was to investigate the potential effect of naturally existing CD11c(low)CD45RB(high) dendritic cells (CD11c(low)CD45RB(high) DCs) on acute severe inflammatory response and mortality rate in burned mice. Changes in the percentage of distinct subsets of splenic DCs and production of cytokines (IL-6, TNF-α, CCL-2) as well as CC chemokine (CCL)-2 were measured by FACS at various time points. The influence of CD11c(low)CD45RB(high) DCs on IL-6, TNF-α, CCL-2 as well as IL-10 levels and mortality rate was observed following a single intraperitoneal injection of DCs to scald mice. Levels of IL-6, CCL-2 and TNF-α were peaked at postburn hours (PBHs) 12, and percentages of CD11c(low)CD45RB(high) DCs were elevated at PBH 12-24. A single intraperitoneal injection of CD11c(low)CD45RB(high) DCs to 15% total body surface area in scald mice led to significant decrease in IL-6, TNF-α and CCL-2, and lethality, but up-regulation of IL-10 compared with untreated mice from PBH 0 to 48. CD11c(low)CD45RB(high) DCs can effectively down-regulate the production of inflammatory cytokines and reduce the mortality rate in 15% TBSA scald injury mice.