Interleukin-37 Attenuates Bleomycin-Induced Pulmonary Inflammation and Fibrosis in Mice

Pulmonary fibrosis is a disease with chronic inflammation and excessive collagen deposition for which there is no effective treatments. Interleukin (IL)-37 is a newly identified anti-inflammatory cytokine but its role in pulmonary fibrosis remains unclear. In this study, we investigated the effect o...

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Veröffentlicht in:Inflammation 2018-10, Vol.41 (5), p.1772-1779
Hauptverfasser: Li, Yan, Gao, Qiaoyan, Xu, Keye, Peng, Xiao, Yuan, Xianli, Jiang, Wenwen, Li, Mingcai
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Sprache:eng
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Zusammenfassung:Pulmonary fibrosis is a disease with chronic inflammation and excessive collagen deposition for which there is no effective treatments. Interleukin (IL)-37 is a newly identified anti-inflammatory cytokine but its role in pulmonary fibrosis remains unclear. In this study, we investigated the effect of IL-37 on bleomycin-induced pulmonary fibrosis in mice. A lentivirus expressing IL-37 was administered intranasally to bleomycin-induced C57BL/6 mice. We found that IL-37 improved the survival of mice and reduced the body weight loss of mice caused by bleomycin. Furthermore, IL-37 significantly attenuated pulmonary inflammatory infiltration and collagen deposition and decreased the hydroxyproline content in bleomycin-treated mice. Finally, IL-37 treatment inhibited the expression of monocyte chemoattractant protein-1, IL-6, and tumor necrosis factor-α, but increased the expression of interferon-γ in lung tissues from bleomycin-challenged mice. Taken together, these results suggest that in vivo expression of IL-37 is useful in preventing pulmonary fibrosis induced by bleomycin and provides a possible therapeutic approach to pulmonary fibrosis diseases.
ISSN:0360-3997
1573-2576
DOI:10.1007/s10753-018-0820-9