Immunological Deficiency Associated With Cigarette Smoke Inhalation by Mice

Esber, Henry J.; Menninger, Florian F.; Bogdén, Arthur E.; Mason, Marcus M.

doi:10.1080/00039896.1973.10666328

Cited by 26 publications

(9 citation statements)

References 2 publications

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“…Short-term exposure to extremely high levels of smoke in a cruder smoking apparatus was shown to exert an immediate depressive effect on systemic antibody responses (22). However, long-term exposure to lower (more "physiological") levels of TS (employing the machine described above; 19) produced changes in humoral immune responsiveness analogous to those observed with SO2 and carbon.…”

Section: Humoral and Cellular Immune Responsesmentioning

confidence: 96%

Environmentally induced changes in immunological function: acute and chronic effects of inhalation of tobacco smoke and other atmospheric contaminants in man and experimental animals.

Holt¹,

Keast²

1977

Bacteriological Reviews

128

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Section: Humoral and Cellular Immune Responsesmentioning

confidence: 96%

Environmentally induced changes in immunological function: acute and chronic effects of inhalation of tobacco smoke and other atmospheric contaminants in man and experimental animals.

Holt¹,

Keast²

1977

Bacteriological Reviews

128

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“…Among various environmental pollutants, cigarette smoke (CS) exposure (active and passive) has been a leading cause of morbidity and mortality associated with many disorders ranging from chronic lung and vascular diseases to oral and lung cancers [1,3]. In addition to containing various bioactive compounds including nicotine and carcinogens, CS exerts immunomodulatory effects resulting in alterations of both innate & adaptive systemic immunity [4–11]. These effects on host immunity are multifaceted involving both pro-inflammatory and suppressive effects.…”

Section: Introductionmentioning

confidence: 99%

Cigarette Smoke Exposure Inhibits Contact Hypersensitivity via the Generation of Platelet-Activating Factor Agonists

Sahu

Petrache

Demark

et al. 2013

The Journal of Immunology

107

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Previous studies have established that pro-oxidative stressors suppress host immunity due to their ability to generate oxidized lipids with PAF-receptor (PAF-R) agonist activity. Although exposure to the pro-oxidative stressor cigarette smoke (CS) is known to exert immunomodulatory effects, little is known regarding the role of platelet-activating factor (PAF) in these events. The current studies sought to determine the role of PAF-R signaling in CS-mediated immunomodulatory effects. We demonstrate that CS exposure induces the generation of a transient PAF-R agonistic activity in the blood of mice. CS exposure inhibits contact hypersensitivity in a PAF-R-dependent manner as PAF-R-deficient mice were resistant to these effects. Blocking PAF-R agonist production either by systemic antioxidants or treatment with serum PAF-acetyl hydrolase enzyme blocked both the CS-mediated generation of PAF-R-agonists and PAF-R dependent inhibition of CHS reactions, indicating a role for oxidized glycerophosphocholines with PAF-R agonistic activity in this process. In addition, cyclooxygenase-2 (COX-2) inhibition did not block PAF-R agonist production but prevented CS-induced inhibition of CHS. This suggests that COX-2 acts downstream of the PAF-R in mediating CS-induced systemic immunosuppression. Moreover, CS-exposure induced a significant increase in the expression of the regulatory T cell reporter gene in FoxP3EGFP mice but not in FoxP3EGFP mice on a PAF-R-deficient background. Finally, Treg depletion via anti-CD25 antibodies blocked CS-mediated inhibition of CHS, indicating the potential involvement of Tregs in CS-mediated systemic immunosuppression. These studies provide the first evidence that the pro-oxidative stressor CS can modulate cutaneous immunity via the generation of PAF-R agonists produced through lipid oxidation.

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“…Clinical investigations have revealed that marijuana impairs lymphocyte responsiveness to mitogens and particulate antigens (17), decreases T-cell rosette formation (6,8), suppresses leukocyte migration (20), and alters alveolar macrophage morphology, function, and mobility (14). We and others have previously documented immunosuppressant activities of A9-tetrahydrocannabinol (THC) and selected congeners in animal models, as evidenced by prolongation of skin allograft survival (16), suppression of lymphocyte reactivity to Tand B-cell mitogens (16), reduction of antibody responsiveness to T-dependent antigens (7,10,11), and depletion of splenic and peripheral nucleated cells (10,16). Our available evidence suggests that possibly all of-he immunosuppressant activities of the cannabinoids reside in their action on T lymphocytes (10,21).…”

mentioning

confidence: 99%

Effects of cannabinoids on host resistance to Listeria monocytogenes and herpes simplex virus

Morahan¹,

Klykken²,

Smith³

et al. 1979

Infect Immun

114

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Previous investigations from our laboratories have demonstrated that cannabinoids possess immunosuppressive properties. The present studies were designed to determine whether these agents decrease host resistance to infections with Listeria monocytogenes and herpes simplex virus type 2. Host resistance was measured by changes in the 50% lethal dose of the pathogen in cannabinoidtreated and control mice. The effect of cannabinoids on resistance to L. monocytogens was dose dependent. Delta-9-tetrahydrocannabinol at doses of 38, 75, and 150 mg/kg suppressed resistance to infection by 10-, 17-, and 657-fold, respectively. Marijuana extract was less active but significantly reduced resistance to L. moncytogenes at all tested doses. Resistance to systemic herpes simplex virus type 2 infection was decreased 96-fold by delta-9-tetrahydrocannabinol, although marijuana extract was inactive. The doses and regimen of treatment with cannabinoids that produced significant decreases in host resistance were similar to those which caused suppression of delayed-type hypersensitivity to sheep erythrocytes. The possible mechanisms and public health aspects of the decreased host resistance produced by marijuana extract and its cannabinoids are discussed.

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Immunological Deficiency Associated With Cigarette Smoke Inhalation by Mice

Cited by 26 publications

References 2 publications

Environmentally induced changes in immunological function: acute and chronic effects of inhalation of tobacco smoke and other atmospheric contaminants in man and experimental animals.

Environmentally induced changes in immunological function: acute and chronic effects of inhalation of tobacco smoke and other atmospheric contaminants in man and experimental animals.

Cigarette Smoke Exposure Inhibits Contact Hypersensitivity via the Generation of Platelet-Activating Factor Agonists

Effects of cannabinoids on host resistance to Listeria monocytogenes and herpes simplex virus

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