Regulation of neutrophil O2- production by neutrophil-endothelial cell interaction via CD11b: its modulation by tumor necrosis factor-alpha (TNF-alpha) and lipopolysaccharide (LPS).
Polymorphonuclear leukocyte-endothelial cell (PMN-EC) adhesion and the O2- production by subsequently triggered polymorphonuclear leukocytes (PMN) must be involved in the development of multiple organ failure at septic inflammatory sites. In this study, the adhesion and O2- production of PMN treated with LPS and serum, were markedly enhanced on the EC monolayer by treatment with TNF-alpha or LPS. However, in the intact EC monolayer, neither adhesion nor O2- production was increased. Monoclonal antibodies (mAb) against CD18, CD11b, and ICAM-1 inhibited PMN-EC adhesion. All antibodies except for anti-CD11b mAb had no effect on O2- production by adhered PMN. Anti-CD11b mAb stimulated O2- production in a PMN cell suspension. The pertussis toxin, an inhibitor of some G-proteins, inhibited this reaction. These findings indicate that the adhesion mediated by CD11b provides the signal for O2- production by PMN. This O2- production may involve a signal transduction mechanism mediated by pertussis toxin-sensitive G-proteins.
Miyabayashi
M
M
Department of Pediatrics, Shinshu University School of Medicine, Matsumoto, Japan.
Yasui
K
K
D002450:Cell Communication / Q000276:immunology; D004730:Endothelium, Vascular / Q000166:cytology / Q000276:immunology*; D006801:Humans; D008070:Lipopolysaccharides / Q000494:pharmacology*; D016177:Macrophage-1 Antigen / Q000097:blood*; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism*; D013481:Superoxides / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D008070:Lipopolysaccharides; D016177:Macrophage-1 Antigen; D014409:Tumor Necrosis Factor-alpha; D013481:Superoxides