美国伊利诺伊大学医学院Ki-Wook Kim研究团队近日取得一项新成果。经过不懈努力，他们的最新研究探明了肺间质巨噬细胞对IL-10的感知可防止细菌生态失调引起的肺部炎症并维持免疫稳态。2025年4月29日出版的《免疫学》杂志发表了这项成果。

该课题组研究人员研究了这种交流以及免疫抑制IL-10信号对肺稳态的影响。该课题组发现间质巨噬细胞（IMs）对IL-10的感知是预防自发性肺炎症所必需的。IMs中IL-10信号的缺失通过激活经典单核细胞和CD4⁺ T细胞亚群引发炎症级联，导致慢性肺部炎症。对抗生素治疗和无菌小鼠的分析证实，缺乏IL-10信号的动物的肺部炎症是由共生细菌引发的。16S rRNA测序结果显示，酸性德尔菲特菌和红红球菌是肺部炎症的潜在驱动因素。鼻内给药这些细菌或移植人类粪便微生物群会引起肺炎症。这些研究结果表明，IMs对IL-10的感知有助于通过预防由共生失调引起的肺部炎症来维持肺内平衡。

据悉，免疫系统和微生物群之间的相互作用对维持免疫稳态至关重要。

附：英文原文

Title: IL-10 sensing by lung interstitial macrophages prevents bacterial dysbiosis-driven pulmonary inflammation and maintains immune homeostasis

Author: Seung Hyeon Kim, Zachary White, Anastasiia Gainullina, Soeun Kang, Jiseon Kim, Joseph R. Dominguez, Yeonwoo Choi, Ivan Cabrera, Madison Plaster, Michihiro Takahama, Rafael S. Czepielewski, Jinki Yeom, Matthias Gunzer, Nissim Hay, Odile David, Nicolas Chevrier, Teruyuki Sano, Ki-Wook Kim

Issue&Volume: 2025-04-29

Abstract: Crosstalk between the immune system and the microbiome is critical for maintaining immune homeostasis. Here, we examined this communication and the impact of immune-suppressive IL-10 signaling on pulmonary homeostasis. We found that IL-10 sensing by interstitial macrophages (IMs) is required to prevent spontaneous lung inflammation. Loss of IL-10 signaling in IMs initiated an inflammatory cascade through the activation of classical monocytes and CD4+ T cell subsets, leading to chronic lung inflammation with age. Analyses of antibiotic-treated and germ-free mice established that lung inflammation in the animals lacking IL-10 signaling was triggered by commensal bacteria. 16S rRNA sequencing revealed Delftia acidovorans and Rhodococcus erythropolis as potential drivers of lung inflammation. Intranasal administration of these bacteria or transplantation of human fecal microbiota elicited lung inflammation in gnotobiotic Il10-deficient mice. These findings highlight that IL-10 sensing by IMs contributes to pulmonary homeostasis by preventing lung inflammation caused by commensal dysbiosis.

DOI: 10.1016/j.immuni.2025.04.004

Source: https://www.cell.com/immunity/abstract/S1074-7613(25)00167-0