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Published ahead of print on December 30, 2003, doi:10.1164/rccm.200210-1154OC

Am. J. Respir. Crit. Care Med., Volume 169, Number 8, April 2004, 903-909

A more recent version of this article appeared on April 15, 2004
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Submitted on October 8, 2002
Accepted on December 30, 2003

Inhibitory Effect of Nicotine on Experimental Hypersensitivity Pneumonitis in vivo and in vitro

Marie-Renee Blanchet1, Evelyne Israel-Assayag1, and Yvon Cormier1*

1 Pneumology, Institut Universitaire de Cardiologie et de Pneumologie de l'Universite Laval, Hopital Laval, Ste-Foy, Quebec, Canada

* To whom correspondence should be addressed. E-mail: yvon.cormier{at}med.ulaval.ca.

The incidence of hypersensitivity pneumonitis (HP) is lower in smokers than in non smokers. Since nicotine is immunosuppressive, we hypothetized that it could have a protective effect on HP induction in vivo. HP was induced in mice which were treated with nicotine either intraperitoneally (IP) (0.5 to 2.0 mg/kg/day) or intranasally (IN) (0.025 to 2.0 mg/kg/day). Both IP and IN treated animals had fewer bronchoalveolar lavage (BAL) total cells and lymphocytes, and a decreased lung tissue inflammation. IFN-{gamma}but not IL-10 mRNA expression was reduced in lung tissue of 2.0 mg/kg IN treated animals. To test the effect of nicotine on alveolar macrophages, AMJ2-C11 cells were treated with nicotine and stimulated with lipopolysaccharide (LPS) or Saccharopolyspora rectivirgula a causative agent of HP. Nicotine reduced TNF release and TNF, IL-10 and IFN-{gamma} mRNA expression following stimulation, and decreased CD80 expression by 55% in LPS stimulated and by 41% in SR stimulated cells. We conclude that nicotine could be, at least in part, responsible for the protection observed in smokers against HP. The inhibitory effect of nicotine on AM could be one of the mechanisms involved.
Key words: alveolar macrophages, nicotine, hypersensitivity pneumonitis, cytokines




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