Cigarette smoke (CS) is a very important cause of pulmonary inflammatory diseases. Interleukin (IL)-35 is a novel anti-inflammatory cytokine but its role in CS-mediated lung inflammation remains unclear. In the present study, we examined the effect of IL-35 expression on CS-induced lung inflammation in mice. A plasmid DNA expressing IL-35 was injected into mice via a hydrodynamic-based gene delivery that were subsequently exposed to CS three times a day for 5 days. We found that IL-35 expression inhibited pulmonary inflammatory infiltration, lung tissue lesions, mucus secretion, and myeloperoxidase activity in CS-treated mice. Moreover, IL-35 expression decreased the production of IL-1β, tumor necrosis factor-α, IL-6, and IL-17, but increased the level of IL-10 in bronchoalveolar lavage fluids and lung tissues from CS-challenged mice. These results suggest that in vivo expression of IL-35 can protect against CS-induced lung inflammation and may be a therapeutic target in CS-related pulmonary diseases.
Keywords: Cigarette smoke; Hydrodynamic-based gene delivery; IL-35; Lung inflammation.
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