Abstract Title:

Chronic self-administration of nicotine in rats impairs T cell responsiveness.

Abstract Source:

J Pharmacol Exp Ther. 2002 Sep;302(3):935-9. PMID: 12183649

Abstract Author(s):

Roma Kalra, Shashi P Singh, Dean Kracko, Shannon G Matta, Burt M Sharp, Mohan L Sopori

Article Affiliation:

Immunology Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Road SE, Albuquerque, NM 87108, USA.


Chronic exposure of rodents to nicotine via subcutaneously or intracerebroventricularly implanted miniosmotic pumps affects T cell function. However, this method of continuous nicotine administration does not replicate the self-motivated administration of nicotine in human smokers. To determine whether nicotine impairs the immune system under conditions pertinent to human smokers, we investigated the T cell responsiveness of male Lewis rats self-administering (SA) nicotine (0.03 mg/kg of body weight per injection) 40 to 50 times/day for 5 weeks, using a model of virtually unlimited access to nicotine. Compared with sham control animals, the concanavalin A-induced proliferation of spleen cells from SA rats was significantly decreased. Moreover, the ability of spleen cells to mobilize intracellular Ca(2+) after ligation of the T cell antigen receptor (TCR) with an anti-alphabeta TCR antibody was significantly less in SA than in control rats. In addition, inositol 1,4,5-trisphosphate (IP(3))-sensitive intracellular Ca(2+) stores were markedly depleted in spleen cells from SA animals. These results suggest that chronic nicotine self-administration suppresses T cell responsiveness, and this suppression may result from an impaired TCR-mediated signaling that stems from the depletion of IP(3)-sensitive intracellular Ca(2+) stores.

Study Type : Animal Study

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