Phagocytosis by emigrated, intra-abdominal neutrophils is depressed during human secondary peritonitis.
The phagocytic function of neutrophils is a crucial element in host defense against invading microorganisms. Patients with diffuse peritonitis depend on adequate reactivity of neutrophils, in particular locally in the peritoneal cavity as well as in the circulation. This study examined phagocytosis as well as numerical expression of Fcgamma I-III (CD16, CD32, CD64) and complement receptors (CD18, CD35) of emigrated, intra-abdominal and circulating neutrophils during human secondary peritonitis using fluorescence-activated cell analysis. Optimally opsonized E. coli bacteria were used independently of the well-known low level of opsonic molecules during peritonitis. Compared with controls (abdominal surgery without peritonitis), the percentage of emigrated neutrophils which engulfed E. coli bacteria was significantly depressed until 48 h after diagnosis of, and surgery for, peritonitis. When patients with complicated peritonitis (septic shock, multiple organ failure) were compared with patients without complications, phagocytosis was even more depressed in patients with complications. Numerical expression of CD64 (Fcgamma RI) and CD35 (CR1) increased significantly on emigrated polymorphonuclear leukocytes (PMNs) during peritonitis when compared to controls. There was no difference in CD18 and CD32 (Fcgamma RII) expression between the two groups. Numerical expression of CD16 (Fcgamma RIII) on emigrated PMNs decreased significantly in peritonitis. This was more pronounced in patients with complicated peritonitis. We conclude that there is a long-lasting depression of phagocytosis by emigrated PMNs during peritonitis, independent of the opsonic activity. Our data suggest that decreased phagocytosis might be correlated to the profound drop in CD16 on these cells.
Holzer
Katharina
K
Department of General Surgery, Johann Wolfgang Goethe University, Frankfurt, Germany. Holzer@em.uni-frankfurt.de
Konietzny
P
P
Wilhelm
Kerstin
K
Encke
A
A
Henrich
D
D
D034841:Abdominal Cavity; D018821:CD18 Antigens / Q000032:analysis; D002465:Cell Movement / Q000276:immunology*; D002470:Cell Survival / Q000276:immunology; D004926:Escherichia coli / Q000276:immunology; D004927:Escherichia coli Infections / Q000276:immunology; D006801:Humans; D009102:Multiple Organ Failure / Q000150:complications; D009504:Neutrophils / Q000737:chemistry / Q000166:cytology / Q000276:immunology*; D010538:Peritonitis / Q000209:etiology / Q000276:immunology* / Q000382:microbiology; D010587:Phagocytosis / Q000276:immunology*; D011951:Receptors, Complement / Q000032:analysis; D017463:Receptors, Complement 3b / Q000032:analysis; D017452:Receptors, IgG / Q000032:analysis; D012772:Shock, Septic / Q000150:complications; D013696:Temperature
D018821:CD18 Antigens; D011951:Receptors, Complement; D017463:Receptors, Complement 3b; D017452:Receptors, IgG