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白细胞介素-37 减轻博来霉素诱导的小鼠肺部炎症和纤维化。

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

机构信息

Department of Immunology, Zhejiang Provincial Key Laboratory of Pathophysiology, Ningbo University School of Medicine, 818 Fenghua Road, Ningbo, 315211, China.

出版信息

Inflammation. 2018 Oct;41(5):1772-1779. doi: 10.1007/s10753-018-0820-9.

Abstract

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.

摘要

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。

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