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Songmin Ying

As seen in: Nature
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Articles

SREBP2 promotes macrophage alternative activation and allergic airway inflammation independent of cholesterol biosynthesis

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By Yinfang Wu, Kua Zheng, Lingling Dong, Shenwei Gao, Yanping Wu, Zhengyuan Liu, Jieyu Li, Haipin Chen, Qingyu Weng, Miao Li Verified, Chen Zhu, Jiahuan Xu, Songmin Ying, Zhihua Chen
| Nature Verified
Abstract Immunometabolic reprogramming is increasingly recognized as a critical regulator of macrophage activation and function. This study aimed to elucidate the role of the SREBP2-cholesterol biosynthetic pathway in M2 activation of interstitial macrophages (IMs) during allergic asthma. We observed a significant expansion of M2-polarized IMs with heightened SREBP2-cholesterol biosynthetic activity in the lungs of asthmatic mice.
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Lysosomal acidity and cathepsin L activate eosinophils via ARG1-mediated arginine metabolism in allergic airway inflammation - Nature Communications

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By Qingyu Weng, Songmin Ying, Zhihua Chen, Fugui Yan
| Nature Verified
Abstract Eosinophils are the predominant immune cells implicated in the pathogenesis of asthma, highlighting the need for strategies to mitigate their effects. While previous studies have implicated the importance of lysosomes in eosinophil function, the precise role of lysosomes in eosinophil activation during asthma remains insufficiently understood. In this study, we demonstrate that lysosomal acidity and cathepsin L activity in eosinophils are elevated in asthmatic patients and mouse models.
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TGF-β signaling promotes eosinophil activation in inflammatory responses - Cell Death & Disease

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By Songmin Ying, Huahao Shen, Zhihua Chen, Qingyu Weng
| Nature Verified
Abstract Eosinophils, traditionally associated with allergic phenomena, play a pivotal role in inflammatory responses. Despite accumulating evidence suggesting their pro-inflammatory function upon activation, the underlying mechanisms governing eosinophil activation remain incompletely characterized. In this study, we investigate the local activation of pulmonary and colon eosinophils within the inflammatory microenvironment.
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