Lm. Napolitano et C. Campbell, POLYMICROBIAL SEPSIS FOLLOWING TRAUMA INHIBITS INTERLEUKIN-10 SECRETION AND LYMPHOCYTE-PROLIFERATION, The journal of trauma, injury, infection, and critical care, 39(1), 1995, pp. 104-111
Immune competence declines following major injury, and predisposes the
trauma patient to infection. Interleukin-10 (IL-10), although an immu
nosuppressive cytokine, is also important in the initiation of immune
responses. This study investigated alterations in IL-10 and immune fun
ction associated with polymicrobial sepsis following trauma using muri
ne femur fracture (FFx) and cecal ligation/puncture (CLP) models. Mice
were randomized to Normal, FFx, Alcohol and FPx (EtOH+FFx), CLP, FFxCLP, and EtOH+FFx+CLP. Polymicrobial sepsis was induced by performing
CLP 4 days after FFx, and animals were killed 14 days later; immune fu
nction was assessed by in vitro splenocyte cultures. Lymphocyte prolif
erative responses were significantly suppressed in FFx and CLP animals
. Splenocyte IL-10 production was significantly reduced in FFx and CLP
animals, with concurrent increases in nitrite and tumor necrosis fact
or release. This study documents that trauma induces alterations in th
e inflammatory cytokine cascade that affect the immune response to sub
sequent septic challenges.