Effects of tobacco smoke on the secretion of interleukin‐1β, tumor necrosis factor‐α, and transforming growth factor‐β from peripheral blood mononuclear cells

Abstract

Alterations of the host response caused by short-term exposure to high levels of smoke during the act of smoking (acute smoke exposure) as well as long-term exposure to lower levels of tobacco substances in the bloodstream of smokers (chronic smoke exposure) may play a role in the pathogenesis of periodontal diseases in smokers. In this study, we examined the secretion of three cytokines [interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and transforming growth factor (TGF)-beta] from mononuclear blood cells from current smokers and non-smokers exposed to in vitro tobacco smoke (which may be comparable to in vivo acute smoke exposure) and mononuclear blood cells from current smokers not exposed to further in vitro smoke (which may be comparable to chronic smoke exposure). Peripheral blood mononuclear cells were isolated from eight healthy current smokers and eight healthy non-smokers, plated in culture wells, exposed in vitro for 1-5 min to cigarette smoke in a smoke box system or not exposed (baseline controls), and then incubated without further smoke exposure for another 24 h. Supernatants from each well were then collected and assayed for the concentrations of the three cytokines by enzyme-linked immunosorbent assay (ELISA). At baseline, mean IL-1beta levels were higher in smokers than in non-smokers (mean: 10.6 vs. 5.9 pg/ml, anova: P < 0.05). In both smokers and non-smokers, secreted levels of IL-1beta increased from 0 to 5 min of in vitro smoke exposure (mean: 5.9-9.9 pg/ml, t-test: P < 0.05 for non-smokers only) with levels in smokers higher than in non-smokers (P > 0.05). Mean TNF-alpha levels increased from 0 to 2 min of smoke exposure and decreased from 2 to 5 min in smokers and non-smokers, with higher levels in non-smokers than smokers at all time-points (P > 0.05). Mean TGF-beta levels were higher in smokers than in non-smokers at all time-points (mean: 180.5 vs. 132.0 pg/ml, P < 0.05 at 5 min only) with no significant alteration of the pattern of secretion with cigarette smoke exposure. These observed alterations in the secretion of cytokines from mononuclear blood cells in smokers, relative to non-smokers, and with in vitro smoke exposure may play a role in the pathogenesis of periodontal diseases in smokers.

Smoking, Metalloproteinases, and Vascular Disease

“…83 Cigarette smoking is associated with increased circulating levels of TNF and IL-1␤ as well as increased monocyte expression of IL-1␤. 84 Nicotine increases PDGF expression from platelets. 85 Nicotine and cotinine directly stimulate VSMC collagenase, stromelysin, and gelatinase expression.…”

Cytokines Elicited by HSP60 in Periodontitis with and without Coronary Heart Disease

“…Exposure to smoking has been associated with reduced release of TNF-α in human alveolar macrophages [48,49]. In this study there was significant difference in the smoking pack years amongst the patient group compared to the gingivitis group ( Table 2).…”

“…The lack of significant association between serum CRP and TNF-α in the gingivitis and ging/CHD groups may simply reflect the complexity of inflammation and its many pathways and HSP60-induced TNF-α may be an indirect association with CRP and that CP induced inflammation drives TNF-α production. There is evidence for this from previous studies showing that CRP and TNF-α are both increased in patients with CP [48][49][50] and reduced following anti-microbial and non-surgical treatment of chronic periodontitis [50].…”

Effect of Smoking on Metalloproteinases (MMPs) Activity in Patients with Acute Myocardial Infarction (AMI)

“…Cigarette smoke may increase MMP expression via activation of inflammatory transcription factors [28]. It is also associated with increased circulating levels of TNF-alpha and IL1beta as well as increased monocyte expression of IL-1beta [29]. Nicotine and cotinine of the cigarette smoke directly stimulates…”