Intratracheal interleukin‐10 administration reduces acute lung injury induced by sulfur dioxide exposure in mice

Therapies capable of reducing acute high‐consequence airborne chemical exposure‐induced lung disease are lacking. This study seeks to determine the therapeutic potential of interleukin (IL)‐10 administered following acute sulfur dioxide (SO 2 ) exposure in mice. C57BL/6 male and female mice were exposed to SO 2 gas at 125 ppm for 4 h and subsequently treated 2–3 h later with IL‐10 (1 μg) or vehicle control by intratracheal instillation for a total of 3 doses over 2 days with comparisons to sham‐treated mice ( N = 20 mice/group). IL‐10 treatment reduced SO 2 ‐induced weight loss with corresponding reductions in SO 2 ‐induced circulating markers of inflammation (pentraxin‐2 and fibrinogen). IL‐10 reduced SO 2 ‐induced markers of lung cell permeability (surfactant protein‐D and protein), and cell death (lactate dehydrogenase [LDH]). SO 2 ‐induced lung infiltrates of neutrophils and activated macrophages were reduced with IL‐10 treatment. IL‐10 reduced SO 2 ‐induced increases in total protein, Substance P, apoptotic cells, post‐translational citrullinated and malondialdehyde‐acetaldehyde‐modified proteins, and vimentin. Compared to female mice, SO 2 exposure led to greater increases in serum pentraxin‐2, fibrinogen, LDH levels, and lavage fluid cells in males. In conclusion, short‐term, intratracheal IL‐10 therapy administered after acute SO 2 exposure favorably modulates acute lung injury consequences to suggest a therapeutic potential to decrease adverse systemic and lung effects.