Smoking and inflammation in laryngeal squamous cell carcinoma

Introduction/Objective Epidemiological studies have established cigarette smoking as one of the most significant risk factors in pathogenesis of laryngeal squamous cell carcinoma (LSCC). One of the possible underlying mechanism is chronic inflammation, but published data regarding the effect of tobacco on systemic immune response is inconsistent. The goal of this study was to evaluate concentrations of serum proinflammatory cytokines [interleukin (IL)-6, IL-1 beta, and tumor necrosis factor (TNF)-alpha] in patients with LSCC and in healthy subjects according to cigarette smoking. Methods Fifty-nine LSCC patients and 44 healthy controls were enrolled in the study. Samples of peripheral blood and details of tobacco use were gathered from the examinees. Flow cytometry was performed to analyze serum concentrations of IL-6, IL-1 beta, and TNF-alpha. The results were compared according to active smoking status. Results Statistical analysis revealed no significant difference between smoking LSCC patients and smoking healthy subjects. Additionally, investigated cytokines were not significantly different in healthy subjects according to smoking status. In non-smoking participants with LSCC, concentrations of serum IL-1 beta and TNF-alpha were higher (p < 0.05) in comparison with smoking LSCC patients. Conclusion Findings of our study may indicate that smoking leads to the suppression of proinflammatory response in LSCC patients, whilst proinflammatory response is unaffected by cigarettes in healthy subjects.