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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Effects of Cigarette Smoke on Immune Response: Chronic Exposure to Cigarette Smoke Impairs Antigen-Mediated Signaling in T Cells and Depletes IP3-Sensitive Ca2+ Stores

Roma Kalra, Shashi P. Singh, Susan M. Savage, Gregory L. Finch and Mohan L. Sopori
Journal of Pharmacology and Experimental Therapeutics April 2000, 293 (1) 166-171;
Roma Kalra
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Shashi P. Singh
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Susan M. Savage
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Gregory L. Finch
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Mohan L. Sopori
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Abstract

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-γ1 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.

Footnotes

  • Send reprint requests to: Mohan Sopori, Ph.D., Pathophysiology Division, Box 5890, Lovelace Respiratory Research Institute, Albuquerque, NM 87185. E-mail: msopori{at}lrri.org

  • ↵1 This work was supported in part by Grant DA04208 from the National Institute of Drug Abuse.

  • Abbreviations:
    SM
    cigarette smoke
    AFC
    antibody-forming cell
    TRC
    T cell antigen receptor
    SRBC
    sheep red blood cells
    PTK
    protein tyrosine kinase
    PLC
    phospholipase C
    IP3
    inositol-1,4,5-trisphosphate
    PY
    phosphotyrosine
    TPM
    total particulate matter
    CON
    control
    FA
    filtered air
    mAb
    monoclonal antibody
    • Received May 18, 1999.
    • Accepted December 6, 1999.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 293 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 293, Issue 1
1 Apr 2000
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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Effects of Cigarette Smoke on Immune Response: Chronic Exposure to Cigarette Smoke Impairs Antigen-Mediated Signaling in T Cells and Depletes IP3-Sensitive Ca2+ Stores

Roma Kalra, Shashi P. Singh, Susan M. Savage, Gregory L. Finch and Mohan L. Sopori
Journal of Pharmacology and Experimental Therapeutics April 1, 2000, 293 (1) 166-171;

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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Effects of Cigarette Smoke on Immune Response: Chronic Exposure to Cigarette Smoke Impairs Antigen-Mediated Signaling in T Cells and Depletes IP3-Sensitive Ca2+ Stores

Roma Kalra, Shashi P. Singh, Susan M. Savage, Gregory L. Finch and Mohan L. Sopori
Journal of Pharmacology and Experimental Therapeutics April 1, 2000, 293 (1) 166-171;
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