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Vol. 293, Issue 1, 166-171, April 2000
Pathophysiology (R.K., S.P.S., S.M.S., M.L.S.) and Toxicology
(G.L.F.) Divisions, Lovelace Respiratory Research Institute,
Albuquerque, New Mexico
Chronic exposure of mice and rats to cigarette smoke affects T-cell
responsiveness that may account for the decreased T-cell proliferative
and T-dependent antibody responses in humans and animals exposed to
cigarette smoke. However, the mechanism by which cigarette smoke
affects the T cell function is not clearly understood. Our laboratory
has shown that chronic exposure of rats to nicotine inhibits the
antibody-forming cell response, impairs the antigen-mediated signaling
in T cells, and induces T cell anergy. To determine the mechanism of
cigarette smoke-induced immunosuppression and to compare it with
chronic nicotine exposure, rats were exposed to diluted, mainstream
cigarette smoke for up to 30 months or to nicotine (1 mg/kg b.wt./24 h)
via miniosmotic pumps for 4 weeks, and evaluated for immunological
function in vivo and in vitro. This article presents evidence
suggesting that T cells from long-term cigarette smoke-exposed rats
exhibit decreased antigen-mediated proliferation and constitutive
activation of protein tyrosine kinase and phospholipase C-
1
activities. Moreover, spleen cells from smoke-exposed and
nicotine-treated animals have depleted
inositol-1,4,5-trisphosphate-sensitive Ca2+ stores and a
decreased ability to raise intracellular Ca2+ levels in
response to T cell antigen receptor ligation. These results suggest
that chronic smoking causes T cell anergy by impairing the antigen
receptor-mediated signal transduction pathways and depleting the
inositol-1,4,5-trisphosphate-sensitive Ca2+ stores.
Moreover, nicotine may account for or contribute to the immunosuppressive properties of cigarette smoke.
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