Nicotine is chemotactic for neutrophils and enhances neutrophil responsiveness to chemotactic peptides.
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.
D002634:Chemotaxis, Leukocyte / Q000187:drug effects*; D003182:Complement C5; D003594:Cytoplasmic Granules / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D009113:Muramidase / Q000097:blood; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology*; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism; D009538:Nicotine / Q000494:pharmacology*; D010196:Pancreatic Elastase / Q000097:blood; D009195:Peroxidase / Q000097:blood; D013268:Stimulation, Chemical; D013481:Superoxides / Q000097:blood
D003182:Complement C5; D013481:Superoxides; D009240:N-Formylmethionine Leucyl-Phenylalanine; D009538:Nicotine; D009195:Peroxidase; D009113:Muramidase; D010196:Pancreatic Elastase