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CCTα and GVI iPLA2-induced aberrant phosphatidylcholine metabolism contributes to pulmonary inflammation and fibrosis

文献类型： 外文期刊

作者： Liu, Tao 1 ; Jia, Hong 1 ; Li, Xinsheng 2 ; Shi, Lijun 1 ; Wang, Jing 1 ; Liu, Meizhen 4 ; Liu, Hailong 1 ; Zhang, Tao 6 ; Zhao, Zhenwen 1 ; Zhao, Xinghui 1 ; Zhao, Zhenwen 1 ;

作者机构： 1.Chinese Acad Agr Sci, Inst Anim Sci, Lab Pharmacobiol, Beijing 100193, Peoples R China

2.Xinyang Agr & Forestry Univ, Coll Anim Husb & Vet Med, Xinyang 464001, Peoples R China

3.Henan Agr Univ, Coll Vet Med, Zhengzhou 450002, Peoples R China

4.East China Normal Univ, Inst Biomed Sci, Shanghai Key Lab Regulatory Biol, Shanghai 200241, Peoples R China

5.East China Normal Univ, Sch Life Sci, Shanghai 200241, Peoples R China

6.Beijing Univ Agr, Coll Anim Sci & Technol, Beijing Key Lab Tradit Chinese Vet Med, Beijing 102206, Peoples R China

7.Chinese Acad Sci, Inst Chem, Beijing Mass Spectrometry Ctr, Key Lab Analyt Chem Living Biosyst, Beijing 100190, Peoples R China

关键词： Lung; Inflammation; Fibrosis; PC; CCT alpha; GVI iPLA2

期刊名称：INTERNATIONAL IMMUNOPHARMACOLOGY （ 影响因子：4.7； 五年影响因子：5.0 ）

ISSN： 1567-5769

年卷期： 2025 年 156 卷

页码：

收录情况： SCI

摘要： To date, no comprehensive profiling of phosphatidylcholine (PC) and lysophosphatidylcholine (LPC) with pulmonary inflammation and fibrosis has been published. Our study aimed to analyze PC and LPC metabolism with the development and persistence of pulmonary inflammation and the progression to fibrosis; and their relationship. Mice and cell models exposed to bleomycin and/or transforming growth factor-(31 (TGF-(31) were developed; and porcine surrogates for pulmonary fibrosis were included. Histopathological, immunofluorescence and immunohistochemical staining, transmission electron microscopy, colorimetric, activity and immune complex (IC) assay, lipidomics analysis; and pharmacological intervention assay were used to analyze PC and LPC profile, pulmonary fibrosis and their relationship. Current evidence suggests that 16:0 20:5 PC is a conserved biomarker; and 16:0 18:1 PC, 16:0 18:2 PC; and 16:0 LPC are the potential targets for this disease. Specifically, 16:0 18:1 PC accumulation and exogenous treatment affected lung cell recruitment, migration, transformation, cross-talk, survival/death; and enhanced profibrotic factor release, IC and extracellular matrix (ECM) deposition, where CTP:phosphocholine cytidylyltransferase alpha (CCT alpha) and group VI Ca2+-independent phospholipase A2 (GVI iPLA2) play an important role, particularly in lung and spleen neutrophils, macrophages, and T lymphocytes. Overall, these results provide new insights into how the dysregulated PC metabolism, particularly for 16:0 18:1 PC, affects the development and persistence of lung inflammation and the progression to fibrosis, and thus may facilitate the discovery of biomarkers and targets for this disease.

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