Introduction: Sarcoidosis is a multiorgan granulomatous disease of unknown etiology. The predominance of Th1‑related cytokines is observed in the bronchoalveolar fluid (BALF) in pulmonary sarcoidosis. Recently, Th17 cells have been postulated to be involved in the pathogenesis of sarcoidosis. Sarcoidosis is more prevalent in nonsmokers than in smokers. The exact effect of smoking on granulomatous inflammation in this disease remains unclear.
Objectives: The aim of the study was to evaluate the Th1/Th2/Th17‑related cytokine concentration in the BALF of patients with pulmonary sarcoidosis in relation to smoking status.
Patients and methods: The study included 74 patients with confirmed pulmonary sarcoidosis. Data on smoking status were available for 61 patients (26 ever‑smokers, 35 never‑smokers; mean 11 ±9.1 pack-years in smokers). The concentrations of interleukin (IL) 17A (IL‑17A), IL‑10, IL‑6, IL‑4, and IL‑2 as well as interferon γ (IFN‑γ) and tumor necrosis factor α (TNF‑α) were measured in BALF supernatants using a flow cytometry method--the Cytometric Bead Array.
Results: The median concentration of IL‑6, IFN‑γ, and IL‑17A (2.19 pg/ml, 1.28 pg/ml, and 6.08 pg/ml, respectively) did not differ significantly between smokers and nonsmokers. TNF‑α, IL‑10, IL‑4 and IL‑2 levels were below the detection limit in most patients. We observed a significant correlation between IFN‑γ concentration and the number of macrophages in BALF (r = 0.66, P <0.05) and between IL‑17A and IL‑6 levels (r = 0.94, P <0.05).
Conclusions: We confirmed a significant role of IL‑6, IFN‑γ, and IL-17A in the local inflammatory response in sarcoidosis. However, the interpretation of the limited number of cytokine measurements should be made with caution. Further studies are needed to explain the effect of smoking on the pathomechanism of inflammation in sarcoidosis.