慢性阻塞性肺疾病（COPD）和其他炎症性肺疾病受卷烟（CS）影响显著加重。新型细胞因子白细胞介素（IL）-41具有免疫调节作用，但其在CS引起的肺炎症中的功能数据有限且不一致。我们的研究旨在调查IL-41对CS引发的肺炎症的保护能力。在这个模型中，小鼠每天接连5天，每天三次吸入六支香烟，每次吸烟1小时，吸烟之间间隔4小时。小鼠在首次接触CS之前一天，腹腔注射IL-41或阴性对照物。在第6天时，用于评估IL-41对CS引发的肺炎症的影响。我们发现，IL-41预处理减轻了肺部炎症浸润和肺组织病变。IL-41预处理还减少了CS引起的体重减轻，降低了支气管肺泡灌洗液中的巨噬细胞数量以及血液中中性粒细胞和单核细胞的百分比。此外，根据免疫组化学确定，IL-41促进了M2巨噬细胞的偏向，而不是M1巨噬细胞。与其对M2偏向的影响一致，IL-41预处理与CS暴露动物的支气管肺泡灌洗液和肺组织中IL-10水平升高以及血清和肺组织中肿瘤坏死因子-α、IL-6和IL -1β的生成量降低相关联。这些发现表明，IL-41在小鼠体内给予治疗剂量时，可以用于治疗CS引起的肺炎症性疾病，因为它抑制了CS引起的肺部炎症。版权所有©2023 Elsevier B.V. 保留所有权利。

Chronic obstructive pulmonary disease (COPD) and other inflammatory lung illnesses are markedly exacerbated by cigarette smoke (CS). The novel cytokine interleukin (IL)-41 has immunoregulatory effects, but data on its function in lung inflammation caused by CS are limited and inconclusive. Our study aimed to investigate the ability of IL-41 to protect against CS-induced lung inflammation in vivo.In this model, mice were exposed to six cigarettes three times daily for 1 h, with 4-hour intervals between exposures, for 5 consecutive days. Mice received an intraperitoneal dose of IL-41 or a negative control 1 day prior to their initial exposure to CS. On day 6, mice were sacrificed to assess the impact of IL-41 on CS-induced lung inflammation.We found that IL-41 pre-treatment alleviated pulmonary inflammatory infiltration and lung tissue lesions. IL-41 pre-treatment also limited CS-induced weight loss, and resulted in lower numbers of macrophages in the bronchoalveolar lavage fluid and lower percentages of neutrophils and monocytes in the blood. Furthermore, it promoted the polarization of M2 macrophages rather than M1 macrophages, as determined by immunohistochemistry. Consistent with its effects on M2 polarization, pre-treatment with IL-41 was associated with higher levels of IL-10 in the bronchoalveolar lavage fluid and lung tissues of CS-exposed animals and lower production of tumor necrosis factor-α, IL-6 and IL-1β in the serum and lung tissues.These findings suggest that IL-41 could be used therapeutically to treat CS-induced lung inflammatory disorders as it inhibits CS-induced pulmonary inflammation when administered in vivo in mice.Copyright © 2023 Elsevier B.V. All rights reserved.