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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].