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Lactobacillus plantarum-Derived Inorganic Polyphosphate Regulates Immune Function via Inhibiting M1 Polarization and Resisting Oxidative Stress in Macrophages

文献类型: 外文期刊

作者: Li, Shuzhen 1 ; Zheng, Aijuan 1 ; Chen, Zhimin 1 ; Wang, Xiaoying 1 ; Chen, Jiang 2 ; Zou, Zhiheng 2 ; Liu, Guohua 1 ;

作者机构: 1.Chinese Acad Agr Sci, Inst Feed Res, Key Lab Feed Biotechnol, Minist Agr & Rural Affairs, Beijing 100081, Peoples R China

2.Jiangxi Acad Agr Sci, Inst Anim Husb & Vet Sci, Jiangxi Prov Key Lab Anim Green & Hlth Breeding, Nanchang 330200, Peoples R China

关键词: inorganic polyphosphate; macrophages; oxidative stress; M1 polarization; immunomodulation

期刊名称:ANTIOXIDANTS ( 影响因子:6.6; 五年影响因子:7.3 )

ISSN:

年卷期: 2025 年 14 卷 4 期

页码:

收录情况: SCI

摘要: Inorganic polyphosphate (PolyP) is a high-molecular-weight polymer that plays multiple roles in regulating immune responses. However, the specific anti-inflammatory mechanisms of bacteria-derived PolyP are unclear. In the present study, PolyP was extracted from Lactobacillus plantarum (L. plantarum), and the chain length was estimated to be approximately 250 Pi residues. The immune regulatory functions of PolyP were investigated using a lipopolysaccharide (LPS)-induced RAW264.7 cell oxidative stress model, and dexamethasone was used as a positive control. The result revealed that both dexamethasone and PolyP were protective against oxidative stress by inhibiting macrophage M1 polarization and the production of several markers, such as nitric oxide (NO), reactive oxygen species (ROS), inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX)-2. In addition, PolyP suppressed inflammation progression by regulating the production of several cytokines, such as interleukin (IL)-1 beta, interferon (INF)-gamma, tumor necrosis factor (TNF)-alpha, and IL-6, and inhibited the expressions of inhibitory kappa B kinase (IKK) alpha, IKK beta, and extracellular regulated protein kinases 2 (ERK2). Conclusively, PolyP derived from L. plantarum has the ability to protect cells from oxidative stress damage by inhibiting M1 polarization in macrophages. These findings provide insights into the function of PolyP and offer support for the potential application of PolyP in immune-related diseases.

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