Differential impact of nicotine on cellular proliferation and cytokine production by LPS-stimulated murine splenocytes

Hakki, Amal; Hallquist, Nora; Friedman, Herman; Pross, Susan

doi:10.1016/s0192-0561(00)00005-9

Cited by 29 publications

(22 citation statements)

References 26 publications

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“…Nicotine was demonstrated to enhance the growth of L. pneumophila and cause a corresponding inhibition of IL-6, TNF-␣, and IL-12 in a murine alveolar macrophage cell line through nAChRs (136). The substance also affects murine splenocyte production of Th1-and Th2-associated cytokines in a differential manner (74,75). Chronic nicotine treatment of rats induces T-cell anergy, depletes intracellular IP3-sensitive Ca 2ϩ stores, and inhibits the antibody-forming cell response and lymphocyte proliferation, which may prevent the animals from developing a protective immune response to microbial pathogens (66,67,101).…”

Section: Nicotine Effects On Resistance To Infectionsmentioning

confidence: 99%

“…Nicotine appears to affect the immune system through nAChRs on cells in CNS and on immune cells similar to opiates and cannabinoids. Nicotine induces glucocorticoids, through the HPA axis, that modify the immune system (29, 80, 216) as well as directly affecting immune cells (74,75,136,167,217). Nicotine was demonstrated to enhance the growth of L. pneumophila and cause a corresponding inhibition of IL-6, TNF-␣, and IL-12 in a murine alveolar macrophage cell line through nAChRs (136).…”

Section: Nicotine Effects On Resistance To Infectionsmentioning

confidence: 99%

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Microbial Infections, Immunomodulation, and Drugs of Abuse

2003

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The use of recreational drugs of abuse has generated serious health concerns. There is a long-recognized relationship between addictive drugs and increased levels of infections. Studies of the mechanisms of actions of these drugs became more urgent with the advent of AIDS and its correlation with abused substances. The nature and mechanisms of immunomodulation by marijuana, opiates, cocaine, nicotine, and alcohol are described in this review. Recent studies of the effects of opiates or marijuana on the immune system have demonstrated that they are receptor mediated, occurring both directly via specific receptors on immune cells and indirectly through similar receptors on cells of the nervous system. Findings are also discussed that demonstrate that cocaine and nicotine have similar immunomodulatory effects, which are also apparently receptor mediated. Finally, the nature and mechanisms of immunomodulation by alcohol are described. Although no specific alcohol receptors have been identified, it is widely recognized that alcohol enhances susceptibility to opportunistic microbes. The review covers recent studies of the effects of these drugs on immunity and on increased susceptibility to infectious diseases, including AIDS

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Section: Nicotine Effects On Resistance To Infectionsmentioning

confidence: 99%

Section: Nicotine Effects On Resistance To Infectionsmentioning

confidence: 99%

Microbial Infections, Immunomodulation, and Drugs of Abuse

2003

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“…Nicotine appears to be one of the major immunomodulatory components of cigarettes, because it has been shown that the treatment of human PBMC with nicotine significantly inhibited the production of IL-2, TNF-␣, and IFN-␥ in response to anti-CD3 stimulation (10). The suppression of LPS-induced murine splenocyte production of IL-6, TNF-␣, and IFN-␥ by concurrent nicotine treatment has also been demonstrated (11,12).…”

Section: Involvement Of Nicotinic Acetylcholine Receptors In Suppressmentioning

confidence: 99%

Involvement of Nicotinic Acetylcholine Receptors in Suppression of Antimicrobial Activity and Cytokine Responses of Alveolar Macrophages to Legionella pneumophila Infection by Nicotine

Matsunaga

Klein

Friedman

et al. 2001

The Journal of Immunology

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Although nicotine is thought to be one of the major immunomodulatory components of cigarette smoking, how nicotine alters the host defense of the lung and, in particular, immune responses of alveolar macrophages, which are critical effector cells in the lung defense to infection, is poorly understood. Nicotinic acetylcholine receptors (nAChRs) are the receptor for nicotine and may be involved in the modulation of macrophage function by nicotine. In this study, therefore, nicotine-induced suppression of antimicrobial activity and cytokine responses of alveolar macrophages mediated by nAChRs to Legionella pneumophila, a causative agent for pneumonia, were examined. The murine MH-S alveolar macrophage cell line cells expressed the messages for α4 and β2 subunits of nAChRs, but not α7 subunits, determined by RT-PCR. The nicotine treatment of MH-S alveolar macrophages after infection with L. pneumophila significantly enhanced the replication of bacteria in the macrophages and selectively down-regulated the production of IL-6, IL-12, and TNF-α, but not IL-10, induced by infection. These effects were completely blocked by a nonselective antagonist, d-tubocurarine, for nAChRs, but not by a selective antagonist, α-bungarotoxin, for α7-nAChRs. Furthermore, the stimulation of nAChRs with another agonist, 1,1-dimethyl-4-phenylpiperazinium iodide, showed the same effects, which were blocked by the antagonist d-tubocurarine, on the bacterial replication and cytokine regulation with that of nicotine. Thus, the results revealed that nAChRs, the major exogenous ligands of which are nicotine, are involved in the regulation of macrophage immune function by nicotine and may contribute to the cigarette-induced risk factors for respiratory infections in smokers.

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“…In this study, we investigated whether there was a difference between CS-exposed and non-CS-exposed mice in the response of AM on lipopolysaccharide (LPS)-induced B lymphocyte proliferation. LPS is a major proinflammatory glycolipid component of the Gram-negative bacteria cell wall [9] and induces specific proliferation in response to mitogen in mouse [10]. To investigate the mechanism of the inhibition of AM-mediated LPS-induced B lymphocyte proliferation in CS-exposed mice, we also evaluated the influence of CS on the generations of superoxide and hydrogen peroxide in AM.…”

Section: Introductionmentioning

confidence: 99%

Alveolar Macrophage from Cigarette Smoke-Exposed Mice Inhibits B Lymphocyte Proliferation Stimulated with LPS

2008

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Background: Smokers have higher incidences of pulmonary diseases. This increased susceptibility may result from cigarette smoke (CS)-induced impairment of the pulmonary immune system. However, the mechanism(s) is not fully understood. Objective: The aim of this study was to investigate the mechanism of the effect of alveolar macrophages (AM) from CS-exposed mice on B lymphocyte proliferation stimulated with bacterial lipopolysaccharide (LPS). Methods: Mice were exposed to CS using a Hamburg smoking machine, and AM were obtained by bronchoalveolar lavage. Lymphocytes were harvested from spleen in normal mice. AM-mediated B lymphocyte proliferation stimulated with LPS was assessed by the ³H-thymidine method, using lymphocytes as responding cells and AM from CS-exposed or non-CS-exposed mice. Generations of superoxide and hydrogen peroxide were analyzed by flow cytometory, using hydroethidine and dichlorofluorescein diacetate. Results: AM from CS-exposed mice significantly inhibited B lymphocyte proliferation stimulated with LPS compared with AM from non-CS-exposed mice. Generations of superoxide and hydrogen peroxide were significantly increased in CS-exposed AM compared with non-CS-exposed AM. Inhibition of B lymphocyte proliferation stimulated with LPS by AM from CS-exposed mice was clearly recovered by superoxide dismutase and catalase. Conclusions: These results suggest that the inhibition by CS-exposed AM of LPS-induced B lymphocyte proliferation may be caused by the increased superoxide and hydrogen peroxide generation of CS. Therefore, these immunological inhibitions by CS could be associated with increased risk of pulmonary diseases.

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Differential impact of nicotine on cellular proliferation and cytokine production by LPS-stimulated murine splenocytes

Cited by 29 publications

References 26 publications

Microbial Infections, Immunomodulation, and Drugs of Abuse

Microbial Infections, Immunomodulation, and Drugs of Abuse

Involvement of Nicotinic Acetylcholine Receptors in Suppression of Antimicrobial Activity and Cytokine Responses of Alveolar Macrophages to Legionella pneumophila Infection by Nicotine

Alveolar Macrophage from Cigarette Smoke-Exposed Mice Inhibits B Lymphocyte Proliferation Stimulated with LPS

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