Tumor necrosis factor-α serum levels in healthy smokers and nonsmokers

Abstract

Background: Tobacco smoking is the most important risk factor for chronic obstructive pulmonary disease (COPD) development. Inhaled cigarette smoke can induce tumor necrosis factor-a (TNF-a) production by alveolar macrophages, which in turn may enhance the production of metalloproteinases (MMPs). MMPs have been involved in mediating airway inflammation and lung destruction. Objectives: We aimed to measure the TNF-a serum levels in healthy heavy smokers and healthy nonsmokers to determine the dose-response relationship based on the cigarette smoke exposure. Subjects and methods:We included in our study 43 healthy heavy smokers and 19 healthy nonsmokers (the control group). The smokers group was classified as less than one pack, one pack, and more than one pack per day. A clinical and paraclinical evaluation was performed in both groups, without any evidence of infection or COPD. The serum levels of TNF-a were assessed by ELISA. Results: The TNF-a serum levels were significantly higher for the group of smokers compared to the group of nonsmokers (P , 0.004). We also noticed an increased TNF-a concentration in the serum of smokers with more than one pack per day compared with those with less than one pack per day (P , 0.03). There was a positive correlation between the serum level of TNF-a and tobacco smoke exposure. Conclusions:The high levels of TNF-a in the serum of smokers suggest an imbalance between the proinflammatory and anti-inflammatory factors as a result of tobacco smoke exposure. The concentration of TNF-a is elevated in the serum of healthy heavy smokers in a cigarette dosedependent manner. We speculate that the serum level of TNF-a might be a useful biomarker for the selection of heavy smokers with a high risk of developing smoke induced pulmonary diseases.

Chronic alcohol and nicotine consumption as catalyst for systemic inflammatory storm and bone destruction in apical periodontitis

“…In the present study, both the Alcohol group and Nicotine group exhibited elevated serum levels of IL‐1β, IL‐6 and TNF‐α, compared to Control group ( p < .05). These findings are consistent with previous studies demonstrating increased levels of these proinflammatory cytokines in individuals exposed to chronic alcohol consumption (Gonzalez‐Quintela et al., 2007; Heberlein et al., 2014) and tobacco smoking (Aldaham et al., 2015; Petrescu et al., 2010). Furthermore, the simultaneous consumption of alcohol and nicotine resulted in even higher levels of IL‐6 and TNF‐α compared to the isolated consumption ( p < .05), indicating a synergistic proinflammatory effect of both substances.…”

Proteome analysis of bronchoalveolar lavage in pulmonary langerhans cell histiocytosis

“…Another function of plastin 2 is protection against TNF-cytotoxicity [ 26 ]. As cigarette smoke may induce production of tumor necrosis factor-alpha (TNF-α) by alveolar macrophages [ 27 ], up-regulation of PLSL2 in BAL of smokers may have a protective role against this pro-inflammatory cytokine. Interestingly in our PLCH patients this mechanism was down-regulated.…”

Ameliorative effects of curcumin and caffeic acid against short term exposure of waterpipe tobacco smoking on lung, heart and kidney in mice

“…Several investigations revealed that tobacco smoke presentation is related with expanded inflammation. It has been discovered that the degree of serum inflammatory marker, for example, TNF-α is altogether higher in smokers contrasted with non-smokers [ 41 , 42 ]. The present research gave experimental evidence that exposure to WPS induces systemic inflammation and oxidative stress.…”