Inhibition of host immunity by fluid and mononuclear cells from healing wounds

Severe trauma impairs host immunity, which in turn renders the host susceptible to infection often terminating in death. This impairment occurs 7 to 14 days after injury, a time when wound healing is at its maximum. We examined the interactions of wound healing to host immunity by studying the in vitro and in vivo immune effects of wound components (i.e., wound fluid [WF] and wound mononuclear cells [WMNC]). Lewis male rats (RT-1(1] weighing 300 to 350 gm underwent 7 cm dorsal skin incisions and subcutaneous placement of polyvinyl alcohol sponges. At 7 and 10 days after wounding, sponges were removed and WF was separated from the cellular elements. The cell suspension was purified to contain 80% to 90% WMNC. Ten percent WF from 7- and 10-day-old wounds inhibits normal thymic lymphocyte blastogenesis to concanavalin A and phytohemagglutinin. Addition of 5 X 10(4) WMNC leads to similar inhibition. WF and WMNC from 10-day-old wounds also inhibit in vitro allogeneic responses tested in one way MLR of Lewis splenocytes with inactivated ACI (RT-1a) spleen cells by 75% to 96% and 85% to 98%, respectively. The inhibitory action of WF is heat resistant (56 degrees C for 30 minutes) and noncytotoxic. In vivo allogeneic responses, tested by grafting ACI skin onto Lewis recipients, were inhibited by intraperitoneal administration of 10-day-old WF (p less than 0.01). We conclude that WF contains factor(s) that inhibit in vitro and in vivo immune responses. WMNC exhibits the same action, suggesting that they may be the source of the WF inhibitory factor(s). These findings may explain host immunosuppression after severe trauma.