Untreated intra-abdominal sepsis: lack of synergism between polymorphonuclear leukocyte (PMN) complement receptors CR1/CR3 and IgG receptor FcRIII.
We have examined the effects of untreated intra-abdominal sepsis on polymorphonuclear leukocyte (PMN) phagocytosis. Phagocytosis was studied in a receptor-specific fashion looking at the interrelationship between FcRIII-, complement receptor (CR1)-, and complement receptor 3 (CR3)-mediated phagocytosis. Twelve swine underwent either sham laparotomy (n = 5) or laparotomy with cecal ligation and incision (n = 7) to induce intra-abdominal sepsis. PMN phagocytosis was assayed on POD 1, 4, and 8. In animals undergoing sham laparotomy, FcRIII-mediated phagocytosis was less than 10% on all days and was augmented with the addition of C3b or C3bi to the target particles (FcR + CR1 or FcR + CR3 greater than FcR alone). In animals undergoing cecal ligation and incision, baseline FcRIII-mediated phagocytosis increased between POD 1 and 4 and fell between POD 4 and 8. No increase in phagocytosis was seen on POD 4 or 8 with the addition of C3b or C3bi to the target particles (FcR + CR1 or FcR + CR3 = FcR alone). Preligation of the FcRIII but not FcRII or FcRI receptor with a monoclonal antibody (3G8) markedly reduced phagocytosis in the animals with intraabdominal sepsis.(ABSTRACT TRUNCATED AT 250 WORDS)
Department of Surgery, Rhode Island Hospital, Providence 02903.
H H
HH
Simms
R
R
D'Amico
K
K
Burchard
D000038:Abscess / Q000276:immunology; D000818:Animals; D003172:Complement C1 / Q000276:immunology; D005260:Female; D016177:Macrophage-1 Antigen; D009504:Neutrophils / Q000276:immunology*; D010538:Peritonitis / Q000276:immunology*; D010587:Phagocytosis; D011951:Receptors, Complement / Q000276:immunology*; D011961:Receptors, Fc / Q000276:immunology*; D013552:Swine
D003172:Complement C1; D016177:Macrophage-1 Antigen; D011951:Receptors, Complement; D011961:Receptors, Fc