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Table 1 Effects of smoking

From: Rheumatoid arthritis and smoking: putting the pieces together

Effect of smoking Details
Immune cells Exposure to cigarette smoke results in the depression of phagocytic and antibacterial functions of alveolar macrophages [6, 7].
  Killing of intracellular bacteria in smokers' alveolar macrophages is impaired [8].
  Owing to smoke condensate, the primary immune response is diminished [9].
  Chronic smoking causes T-cell anergy [10, 15].
  Nicotinic acetylcholine receptor is involved in the suppression of antimicrobial activity [16].
  Nicotine decreases the induction of antigen-presenting cell-dependent T-cell responses in dendritic cells [10].
  Nicotine attenuates neutrophil functions such as superoxide production [10].
Cytokine production Due to smoke exposure, lipopolysaccharide-induced TNF secretion of alveolar macrophages from experimental animals is decreased [11, 12].
  Smokers' alveolar macrophages release less TNFα, IL-1 and IL-6 [13, 14].
  Nicotine decreases the production of IL-12 in dendritic cells [10].
  Nicotinic acetylcholine receptor is involved in the downregulation of IL-6, IL-12, and TNFα [16].
  Acetylcholine attenuates the release of TNF, IL-1 and IL-6 in lipopolysaccharide-induced human macrophage cultures [17].
  Hydroquinone causes suppression in the production of IL-1, IFNγ and TNFα in human macrophages [19].
  Hydroquinone inhibits IFNγ secretion in lymphocytes [20].
  Unsaturated aldehydes evoke the release of IL-8 and TNFα in human macrophages [21].
Oxidative stress Smoke contains high amounts of free radicals.
  Smoke induces the depletion of intracellular glutathione, resulting in cell injury [23].
  Owing to smoking, redox-sensitive NF-κB and activator protein-1 are activated [22].
  Activator protein-1 is a cis-acting factor bound to the promoter of PAD4 [27].
  Agents, acting on cysteine sulfhydril groups, inactivate peptidyl arginine deiminase, while reduced compounds enhance its activity [28].
  Peptidyl arginine deiminase expression and activity are increased in the lungs of smokers [29].
Anti-estrogenic effect Smoking has an anti-estrogenic effect through the formation of inactive estrogens [30].
Fibrinogen Smokers have higher levels of serum fibrinogen [31].