Department of Immunology, Zhejiang Provincial Key Laboratory of Pathophysiology, Ningbo University School of Medicine, 818 Fenghua Road, Ningbo, 315211, China.
Inflammation. 2018 Oct;41(5):1772-1779. doi: 10.1007/s10753-018-0820-9.
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.
肺纤维化是一种慢性炎症和胶原过度沉积的疾病，目前尚无有效的治疗方法。白细胞介素 (IL)-37 是一种新发现的抗炎细胞因子，但它在肺纤维化中的作用尚不清楚。在这项研究中，我们研究了 IL-37 对博来霉素诱导的小鼠肺纤维化的影响。通过鼻腔内给予表达 IL-37 的慢病毒，对博来霉素诱导的 C57BL/6 小鼠进行处理。我们发现，IL-37 提高了小鼠的存活率，并减轻了博来霉素引起的小鼠体重减轻。此外，IL-37 显著减弱了肺脏炎症浸润和胶原沉积，并降低了博来霉素处理小鼠的羟脯氨酸含量。最后，IL-37 治疗抑制了博来霉素攻击小鼠肺组织中单核细胞趋化蛋白-1、IL-6 和肿瘤坏死因子-α的表达，但增加了干扰素-γ的表达。总之，这些结果表明，体内表达 IL-37 可有效预防博来霉素诱导的肺纤维化，并为肺纤维化疾病提供了一种可能的治疗方法。
