title: Impaired cell-mediated immunity in experimental abdominal sepsis and the effect of interleukin 2.
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.
authors.affiliation: Department of Surgery, Brigham and Women's Hospital-Harvard Medical School, Boston, MA 02115.
authors.forename: D B
authors.initials: DB
authors.lastname: Gough
authors.forename: A
authors.initials: A
authors.lastname: Jordan
authors.forename: J A
authors.initials: JA
authors.lastname: Mannick
authors.forename: M I
authors.initials: MI
authors.lastname: Rodrick
mesh_terms: D000005:Abdomen; D000818:Animals; D001424:Bacterial Infections / Q000209:etiology / Q000276:immunology / Q000401:mortality / Q000628:therapy*; D003208:Concanavalin A / Q000494:pharmacology; D004195:Disease Models, Animal; D004341:Drug Evaluation; D006801:Humans; D007111:Immunity, Cellular / Q000187:drug effects; D007376:Interleukin-2 / Q000627:therapeutic use*; D008297:Male; D051379:Mice; D008805:Mice, Inbred A; D010835:Phytohemagglutinins; D011994:Recombinant Proteins / Q000627:therapeutic use; D013997:Time Factors
chemical_list: D007376:Interleukin-2; D010835:Phytohemagglutinins; D011994:Recombinant Proteins; D003208:Concanavalin A