Publication Date:
1984-01-13
Description:
Neutrophils contribute to chronic bronchitis and pulmonary emphysema associated with cigarette smoking. Nicotine was found to be chemotactic for human neutrophils but not monocytes, with a peak activity at approximately 31 micromolar. In lower concentrations (comparable to those in smokers' plasma), nicotine enhanced the response of neutrophils to two chemotactic peptides. In contrast to most other chemoattractants for neutrophils, however, nicotine did not affect degranulation or superoxide production. Nicotine thus may promote inflammation and consequent lung injury in smokers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Totti, N 3rd -- McCusker, K T -- Campbell, E J -- Griffin, G L -- Senior, R M -- HL16118/HL/NHLBI NIH HHS/ -- HL29594/HL/NHLBI NIH HHS/ -- HL30341/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1984 Jan 13;223(4632):169-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6318317" target="_blank"〉PubMed〈/a〉
Keywords:
Chemotaxis, Leukocyte/*drug effects
;
Complement C5
;
Cytoplasmic Granules/metabolism
;
Dose-Response Relationship, Drug
;
Muramidase/blood
;
N-Formylmethionine Leucyl-Phenylalanine/*pharmacology
;
Neutrophils/*drug effects/metabolism
;
Nicotine/*pharmacology
;
Pancreatic Elastase/blood
;
Peroxidase/blood
;
Stimulation, Chemical
;
Superoxides/blood
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
