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David B. Gough, MCh, FRCS(I); Andrea Jordan; John A. Mannick, MD; Mary L. Rodrick, PhD

Arch Surg. 1992;127(7):859-863.

Abstract
• 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)

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

Footnotes
Accepted for publication October 5, 1991.

Reprint requests to Department of Surgery, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115 (Dr Rodrick).

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