title: Neutrophil priming by cigarette smoke condensate and a tobacco anti-idiotypic antibody.
abstract: A polyphenol-rich reagent, referred to as CSC, was isolated from cigarette smoke condensate and shown to prime purified human neutrophils. A mouse monoclonal anti-idiotypic antibody directed against the polyphenol-reactive determinants on a rabbit polyclonal anti-tobacco glycoprotein antibody was generated and shown to also prime neutrophils. After priming by CSC or tobacco anti-idiotypic antibody, there was a 2.5-fold to threefold increase in CD11b/18 expression and doubling of the number of formyl-methionyl-leucyl-phenylalanine receptors on the cells. The primed cells showed a twofold increase, compared with unprimed cells, in production of superoxide and release of neutrophil elastase after stimulation with formyl-methionyl-leucyl-phenylalanine. Neutrophils in peripheral blood of cigarette smokers have been shown to be primed and more responsive to activating agents. The priming effects attributed to whole cigarette smoke have been demonstrated in these studies using purified neutrophils and CSC or tobacco anti-idiotypic antibody. These studies are a first step in testing the hypothesis that the inflammatory process contributing to progression of chronic obstructive pulmonary disease in ex-smokers may be driven, in part, by tobacco anti-idiotypic antibodies. This hypothesis is novel and carries with it the implication of a heretofore unrecognized autoimmune component in the disease process manifested through production of anti-idiotypic antibodies with tobacco-like activity.
authors.affiliation: Department of Pathology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA. skoethe@mcw.edu
authors.forename: S M
authors.initials: SM
authors.lastname: Koethe
authors.forename: J R
authors.initials: JR
authors.lastname: Kuhnmuench
authors.forename: C G
authors.initials: CG
authors.lastname: Becker
mesh_terms: D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D004789:Enzyme Activation / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D007130:Immunoglobulin Idiotypes / Q000276:immunology*; D019272:Leukocyte Elastase / Q000378:metabolism; D016177:Macrophage-1 Antigen / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects* / Q000502:physiology*; D010766:Phosphorylation / Q000187:drug effects; D011725:Pyridines / Q000494:pharmacology; D044042:Receptors, Formyl Peptide; D011971:Receptors, Immunologic / Q000378:metabolism; D018000:Receptors, Peptide / Q000378:metabolism; D012709:Serum Albumin / Q000378:metabolism; D012906:Smoke; D013481:Superoxides / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases
chemical_list: D000911:Antibodies, Monoclonal; D004791:Enzyme Inhibitors; D007093:Imidazoles; D007130:Immunoglobulin Idiotypes; D016177:Macrophage-1 Antigen; D011725:Pyridines; D044042:Receptors, Formyl Peptide; D011971:Receptors, Immunologic; D018000:Receptors, Peptide; D012709:Serum Albumin; D012906:Smoke; D013481:Superoxides; D009240:N-Formylmethionine Leucyl-Phenylalanine; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D019272:Leukocyte Elastase; C093642:SB 203580