title: Intraabdominal sepsis: enhanced autooxidative effect on polymorphonuclear leukocyte cell surface receptor expression.
abstract: We investigated the effects of untreated intraabdominal sepsis on the interrelationship between PMN oxidative metabolism and cell surface receptor expression. Female swine underwent either sham laparotomy (n = 7) or cecal ligation and incision (n = 9) with assays conducted on postoperative days (POD) 0, 1, 4, and 8. Superoxide anion production, intracellular H2O2 production, and the cell surface expression of Fc gamma RII, III, CR1, and CR3 were measured. In addition, phagocytosis of serum-opsonized zymosan was used as a multivalent ligand for CR3 and subsequently Fc gamma RII, III, and CR1 expression were assayed to determine if intraabdominal sepsis induces a linkage between complement and Fc gamma receptor expression. Superoxide anion production increased between POD 0 and 4 and fell between POD 4 and 8 in animals with untreated intraabdominal sepsis. Intracellular H2O2 production rose between POD 0 and 1 and then fell progressively in animals with untreated intraabdominal sepsis. Simulation of the oxidative burst using glucose/glucose oxidase reduced Fc gamma RII and III expression in both sets of animals with a greater reduction seen by POD 4 in animals with intraabdominal sepsis. CR1/CR3 expression was increased with glucose/glucose oxidase by POD 4 in the presence of intraabdominal sepsis. Xanthine/xanthine oxidase did not alter cell surface receptor expression. Phagocytosis of serum-opsonized zymosan decreased subsequent Fc gamma RII expression in animals with intraabdominal sepsis by POD 4.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Surgery, Rhode Island Hospital, Providence, RI 02903.
authors.forename: H H
authors.initials: HH
authors.lastname: Simms
authors.forename: R
authors.initials: R
authors.lastname: D'Amico
authors.forename: K W
authors.initials: KW
authors.lastname: Burchard
mesh_terms: D000005:Abdomen; D000818:Animals; D000943:Antigens, Differentiation / Q000378:metabolism; D003172:Complement C1 / Q000378:metabolism; D005260:Female; D006861:Hydrogen Peroxide / Q000378:metabolism; D066298:In Vitro Techniques; D007239:Infections / Q000276:immunology* / Q000378:metabolism*; D016177:Macrophage-1 Antigen / Q000378:metabolism; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism*; D010084:Oxidation-Reduction; D010587:Phagocytosis; D011951:Receptors, Complement / Q000378:metabolism; D011961:Receptors, Fc / Q000378:metabolism; D017452:Receptors, IgG; D013481:Superoxides / Q000378:metabolism; D013552:Swine
chemical_list: D000943:Antigens, Differentiation; D003172:Complement C1; D016177:Macrophage-1 Antigen; D011951:Receptors, Complement; D011961:Receptors, Fc; D017452:Receptors, IgG; D013481:Superoxides; D006861:Hydrogen Peroxide