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July 1992

Impaired Cell-Mediated Immunity in Experimental Abdominal Sepsis and the Effect of Interleukin 2

Author Affiliations

From the Department of Surgery, Brigham and Women's Hospital—Harvard Medical School, Boston, Mass.

Arch Surg. 1992;127(7):859-863. doi:10.1001/archsurg.1992.01420070123022

• A murine model of experimental sepsis, ie, cecal ligation and puncture, was used to determine the potential effects of infection on in vitro cell-mediated immunity. Following cecal ligation and puncture, in vitro responses of mouse splenocytes to mitogens (phytohemagglutinin and concanavalin A), the effects of in vitro interleukin 2 on these responses, and the impact of in vivo interleukin 2 on survival were studied. Compared with controls (sham cecal ligation and puncture), phytohemagglutinin responses 1 day after cecal ligation and puncture were enhanced (43%±17%, n = 9), phytohemagglutinin and concanavalin A responses at day 4 were suppressed (45.5%±4.4% and 57.5%±5.6%), and, by day 7, phytohemagglutinin and concanavalin A responses were approaching values in mice treated by sham cecal ligation and puncture. Suppressed phytohemagglutinin responses at day 4 after cecal ligation and puncture were restored to normal with in vitro interleukin 2 (61 052±3407 cpm for cecal ligation and puncture and 64 643±4727 cpm for sham cecal ligation and puncture). Mortalities following cecal ligation and puncture were identical at day 1 after cecal ligation and puncture (6/20) for both interleukin 2–and vehicle-treated groups; thereafter, interleukin 2–treated groups fared better. At day 1 after cecal ligation and puncture, the mean spleen cell phytohemagglutinin response was enhanced (43.8%±17%, n=9) compared with sham cecal ligation and puncture (= 10). By day 4, the responses to both concanavalin A and phytohemagglutinin were suppressed (45.5%±4.4% and 57.5%±5.6%, respectively). Responses at day 7 approached those of controls given sham cecal ligation and puncture. Sepsis causing a temporary impairment of cell-mediated immunity may be a factor in the frequent coexistence of altered cell-mediated immunity and sepsis, and interleukin 2 may have a role in limiting the adverse effects of sepsis.

(Arch Surg. 1992;127:859-863)