Table 1

Effects of smoking

Effect of smoking


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].


Smokers have higher levels of serum fibrinogen [31].

Baka et al. Arthritis Research & Therapy 2009 11:238   doi:10.1186/ar2751