Modulation of in vitro immunoglobulin synthesis of human peripheral blood mononuclear cells by nicotine and cotinine

Fischer, Alain; König, Wolfgang

doi:10.1007/bf00189319

Cited by 15 publications

(9 citation statements)

References 17 publications

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“…Both catecholamines (Alanko et al 1992) and serotonin (Sih et al 1970) can increase eicosanoid synthesis. Nicotine increases the production of proinflammatory cytokines (Fischer and König 1994), which have been reported to augment the expression of 5-lipoxygenase and cyclooxygenases (Serhan et al 1996).…”

Section: Discussionmentioning

confidence: 99%

Effects of smoking cessation and nicotine substitution on systemic eicosanoid production in man

Saareks

Ylitalo

Alanko

et al. 2001

Naunyn-Schmiedeberg's Archives of Pharmacology

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This study investigated the effects of smoking cessation with and without nicotine substitution on the excretion of major urinary metabolites of thromboxane A2 and prostacyclin, 11-dehydrothromboxane B2 and 2,3-dinor-6-ketoprostaglandin F1alpha, respectively, as well as on the excretion of leukotriene E4 in man. Urine samples were obtained from 20 healthy non-smoking controls and from 60 healthy smoking volunteers before, and 3, 7 and 14 days after smoking cessation. Fifteen smokers quit smoking without nicotine substitution, 15 used nicotine chewing gum and 30 used nicotine patches as a substitution therapy. Urinary thiocyanate as well as cotinine and trans-3'-hydroxycotinine excretions were used as compliance and nicotine substitution indicators. 11-Dehydrothromboxane B2, 2,3-dinor-6-ketoprostaglandin F1alpha and leukotriene E4 excretion was about two, three and five times higher in smokers than in controls, respectively. Three days after smoking cessation without nicotine substitution, 11-dehydrothromboxane B2 and 2,3-dinor-6-ketoprostaglandin F1alpha levels were lowered to 75% (P<0.01) and 80% (P<0.05) of the initial values, and after 14 days to 50% (P<0.01) and 60% (P<0.05), respectively. In 3 days leukotriene E4 excretion was dropped to 70% of the initial value (P<0.05), but no further decrease was observed during the study. In individuals using nicotine chewing gum or nicotine patches no significant changes were observed in the analytes during the 2-week follow-up. The increased systemic eicosanoid synthesis observed in smokers may be involved in the harmful cardiovascular effects of smoking. The fact that eicosanoid production remains at pre-cessation level in volunteers who quit smoking but use nicotine substitution may be involved in the risk of cardiovascular complications reported during nicotine replacement therapy.

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Section: Discussionmentioning

confidence: 99%

Effects of smoking cessation and nicotine substitution on systemic eicosanoid production in man

Saareks

Ylitalo

Alanko

et al. 2001

Naunyn-Schmiedeberg's Archives of Pharmacology

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“…Both nicotine and cotinine induce increased production of IL-Ix, IL-2, IL-3, IL-4, and 8 (4) IL-6 in vitro without an effect on IgE production or classswitching (Fischer and Konig, 1994). Increases in serum IL-2 receptor have been noted in smokers compared with non-smokers (Tollerud et al, 1992).…”

Section: Effects Of Tobacco and Smoking On Levels Of The Cytokine Thamentioning

confidence: 97%

Tobacco and Smoking: Environmental Factors That Modify the Host Response (Immune System) and Have an Impact On Periodontal Health

Barbour

Nakashima

Zhang

et al. 1997

Critical Reviews in Oral Biology & Medicine

233

182

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This review summarizes the current data on the effects of smoking and tobacco on the immune system and its potential impact on periodontal health. Smokers are 2.5-6 times more likely to develop periodontal disease than non-smokers, and there is evidence for a direct correlation between the number of cigarettes smoked and the risk of developing disease. Tobacco users also tend to exhibit increased severity of periodontal disease. Direct correlations between tobacco use and increased attachment loss and pocket depth and reduced bone crest height have been reported. Although the correlation between tobacco use and periodontal disease is quite strong, the role of tobacco in the pathogenesis of periodontal disease is uncertain. Recent studies indicate that one potential mechanism is that tobacco use exacerbates periodontal disease because it alters the immune response to periodontal pathogens. Indeed, smokers exhibit increased numbers of peripheral blood mononuclear phagocytes which appear to be functionally compromised. Inadequate phagocyte activity could reduce the clearance of pathogens from the oral cavity and thereby facilitate the development of periodontal disease. Tobacco-exposed B- and T-lymphocytes exhibit reduced proliferative capacities which could limit the production of protective immunoglobulins against oral pathogens. The risk factors for periodontal disease can be broadly classified as genetic, environmental, host-response factors, and host-related factors such as age. Tobacco, an environmental factor, undermines the host response and may facilitate the development and progression of periodontal disease. This review highlights the inter-relatedness of two of the risk factors associated with periodontal disease.

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“…A possible role for the SAM is also proposed in the plasma IL-6 response to some stressors [6,7]. It has been reported that lymphocytes have nicotinic acetylcholine receptors [26], and that nicotine induces IL-6 production in peripheral blood mononuclear cells in vitro [27]. It thus seems possible that the nicotinic mechanism in immune cells, which might also be blocked by chlorisondamine, is involved in the IL-6 response.…”

Section: Research Articlesmentioning

confidence: 99%

Central IL-1 differentially regulates peripheral IL-6 and TNF synthesis

Kitamura¹,

Okamoto²,

Shimamoto

et al. 1998

CMLS, Cell. Mol. Life Sci.

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Centrally given interleukin (IL)-1 is known to induce a rapid rises in blood IL-6. To extend this and to examine the mechanism by which this occurs, the effects of intracerebroventricular (i.c.v.) injection of human recombinant IL-1 beta on mRNA expression of IL-6 and tumour necrosis factor (TNF) in the spleen and liver were examined in rats. I.c.v. injection of IL-1 produced a rapid rise of the tissue mRNA levels of Il-6 and TNF in both organs, prior to and/or in parallel with an increase in their serum levels. Pretreatment with chlorisondamine, a ganglionic blocking agent, inhibited the Il-6 responses, while it had little influence on the TNF responses. The results suggest that brain IL-1 induces peripheral production of IL-6, but not of TNF, through autonomic nervous system activation.

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Modulation of in vitro immunoglobulin synthesis of human peripheral blood mononuclear cells by nicotine and cotinine

Cited by 15 publications

References 17 publications

Effects of smoking cessation and nicotine substitution on systemic eicosanoid production in man

Effects of smoking cessation and nicotine substitution on systemic eicosanoid production in man

Tobacco and Smoking: Environmental Factors That Modify the Host Response (Immune System) and Have an Impact On Periodontal Health

Central IL-1 differentially regulates peripheral IL-6 and TNF synthesis

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