Nicotine exposure alters in vivo human responses to endotoxin

Summary The alpha 7 nicotinic receptor is reportedly a key element in the cholinergic anti‐inflammatory pathway. Because a prototypical ligand for this receptor is nicotine, we studied the in vivo human response to bacterial endotoxin or lipopolysaccharide (LPS) in the context of nicotine or placebo...

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Bibliographic Details
Published in:Clinical and experimental immunology 2007-01, Vol.147 (1), p.28-34
Main Authors: Wittebole, X., Hahm, S., Coyle, S. M., Kumar, A., Calvano, S. E., Lowry, S. F.
Format: Article
Language:English
Subjects:
Administration, Cutaneous
Adolescent
Adult
Analysis of Variance
Biological and medical sciences
Biomarkers - blood
Clinical Studies
Cotinine - blood
Cytokines - blood
E-Selectin - blood
Endotoxins - pharmacology
Fundamental and applied biological sciences. Psychology
Fundamental immunology
human
Humans
Hydrocortisone - blood
Immunopathology
Inflammation
lipopolysaccharide
Lipopolysaccharides - pharmacology
Male
Medical sciences
neuroimmunology
nicotine
Nicotine - pharmacology
Nicotinic Agonists - pharmacology
Prospective Studies
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Summary:Summary The alpha 7 nicotinic receptor is reportedly a key element in the cholinergic anti‐inflammatory pathway. Because a prototypical ligand for this receptor is nicotine, we studied the in vivo human response to bacterial endotoxin or lipopolysaccharide (LPS) in the context of nicotine or placebo pretreatment. Twelve adult male normal subjects were studied prospectively. Six received overnight transcutaneous nicotine administration by application of a standard patch (7 mg). Six hours later, all subjects were given an intravenous dose of endotoxin (2 ng/kg) and were evaluated for an additional 24 h for circulating levels of inflammatory biomarkers, vital signs and symptoms. The nicotine subjects had elevated blood levels of the nicotine metabolite, continine, prior to and throughout the 24‐h post‐endotoxin exposure phase. Subjects receiving nicotine exhibited a significantly lower temperature response as well as attenuated cardiovascular responses for 2·5–6 h after LPS exposure. In addition, increased circulating interkeukin (IL)‐10 and cortisol levels were also noted in nicotine subjects. These data indicate an alteration in LPS‐induced systemic inflammatory responses in normal subjects exposed to transcutaneous nicotine. In this model of abbreviated inflammation, nicotine exposure attenuates the febrile response to LPS and promotes a more prominent anti‐inflammatory phenotype.
ISSN:0009-9104
1365-2249
DOI:10.1111/j.1365-2249.2006.03248.x