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 (SO2) exposure in mice. C57BL/6 male and female mice were exposed to SO2 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 SO2-induced weight loss with corresponding reductions in SO2-induced circulating markers of inflammation (pentraxin-2 and fibrinogen). IL-10 reduced SO2-induced markers of lung cell permeability (surfactant protein-D and protein), and cell death (lactate dehydrogenase [LDH]). SO2-induced lung infiltrates of neutrophils and activated macrophages were reduced with IL-10 treatment. IL-10 reduced SO2-induced increases in total protein, Substance P, apoptotic cells, post-translational citrullinated and malondialdehyde-acetaldehyde-modified proteins, and vimentin. Compared to female mice, SO2 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 SO2 exposure favorably modulates acute lung injury consequences to suggest a therapeutic potential to decrease adverse systemic and lung effects.