title: Surface receptor mobilization in complement-mediated neutrophil activation: characterization and effects of methylprednisolone.
abstract: Complement-mediated neutrophil activation (CMNA) is an important host defense mechanism that is essential for effective neutrophil (PMN) proinflammatory activity. It has also been implicated as a pathogenic mechanism contributing toward the development of adult respiratory distress syndrome. Utilizing zymosan-activated serum pretreatment as an in vitro model for CMNA, we characterized the effects of CMNA on PMN superoxide (SO) production and N-formyl-methionyl-leucyl-phenylalanine (FMLP) receptor status. CMNA was associated with a 132 +/- 38% increase in FMLP-induced SO generation and a 110 +/- 30% increase in FMLP receptor expression. Methylprednisolone pretreatment prevented both the FMLP receptor mobilization and the SO priming effects of CMNA. These data support a concept that FMLP receptor mobilization is an important element in the PMN activation process. In addition, blocking this phenomenon may have clinical significance in attempts to modulate the potential damaging effects of the increased PMN oxidative metabolism associated with CMNA.
mesh_terms: D003165:Complement System Proteins / Q000276:immunology*; D006801:Humans; D008213:Lymphocyte Activation / Q000187:drug effects; D008775:Methylprednisolone / Q000494:pharmacology*; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000276:immunology*; D044042:Receptors, Formyl Peptide; D011971:Receptors, Immunologic / Q000378:metabolism*; D012128:Respiratory Distress Syndrome / Q000097:blood / Q000276:immunology; D013481:Superoxides / Q000097:blood; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
chemical_list: D044042:Receptors, Formyl Peptide; D011971:Receptors, Immunologic; D013481:Superoxides; D009240:N-Formylmethionine Leucyl-Phenylalanine; D003165:Complement System Proteins; D013755:Tetradecanoylphorbol Acetate; D008775:Methylprednisolone