title: Trauma peptide induction of lymphocyte changes predictive of sepsis.
abstract: Post-trauma immunosuppression is characterized by T-cell subpopulation changes and the presence of a low molecular weight suppressive active peptide (SAP), which suppresses T-cell blastogenesis and neutrophil chemotaxis. This study evaluated post-trauma T-cell antigens and suppressive active peptide/T-cell interactions to determine if the suppressive active peptide concentrations predictive of sepsis can cause changes in antigen expression predictive of sepsis. Human lymphocyte markers and differentiation antigens were analyzed post-trauma using flow cytometry for markers predictive of sepsis. Changes induced by purified suppressive active peptide incubated with normal human lymphocytes were similarly analyzed by flow cytometry. SAP concentrations for incubation were chosen which correlated with concentrations in patients developing clinical sepsis. Significant T-cell changes in patients who developed sepsis include: decreased total T-cells, decreased helper cells, decreased natural killer cells, increased Ia expressing mononuclear cells, increased activated T-cells, (L22) and increased IL-2 expressing cells (TAC). Suppressive active peptide can activate T-cells and cause significant increased expression of IL-2 receptors and natural killer cells. Other T-cell changes following trauma predictive of sepsis seem to occur independent of in vitro incubation with suppressive active peptides. IL-2 expressing cells are known to be more readily suppressed by the suppressive peptide. Suppressive peptide activation and subsequent inhibition of T-cells suggests a potential way to explain suppressive peptide-induced immunosuppression following trauma.
authors.affiliation: Department of Surgery, University of California, San Diego 92103.
authors.forename: D B
authors.initials: DB
authors.lastname: Hoyt
authors.forename: A N
authors.initials: AN
authors.lastname: Ozkan
authors.forename: J L
authors.initials: JL
authors.lastname: Ninnemann
authors.forename: J F
authors.initials: JF
authors.lastname: Hansbrough
authors.forename: E
authors.initials: E
authors.lastname: Pinney
authors.forename: S
authors.initials: S
authors.lastname: Wormsley
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal; D000945:Antigens, Differentiation, T-Lymphocyte / Q000276:immunology*; D005434:Flow Cytometry; D006801:Humans; D007108:Immune Tolerance; D008297:Male; D008875:Middle Aged; D009104:Multiple Trauma / Q000276:immunology*; D011446:Prospective Studies; D013491:Suppressor Factors, Immunologic / Q000276:immunology*; D013601:T-Lymphocytes / Q000145:classification* / Q000276:immunology; D014946:Wound Infection / Q000276:immunology*; D014949:Wounds, Nonpenetrating / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D000945:Antigens, Differentiation, T-Lymphocyte; D013491:Suppressor Factors, Immunologic