Essential Fatty Acids and Their Metabolites in the Pathobiology of Inflammation and Its Resolution.
Essential Fatty Acids and Their Metabolites in the Pathobiology of Inflammation and Its Resolution.
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DOI：
10.3390/biom11121873
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发表时间：
2021-12-14
期刊：
影响因子：
5.5
通讯作者：
Das UN
中科院分区：
文献类型：
--
作者：
Das UN
花生四烯酸（AA）的代谢在炎症的开始和消退中是至关重要的。前列腺素E2 （PGE2）和白三烯B4/D4/E4 （LTB4/LD4/LTE4）来源于AA，参与炎症的启动和免疫反应、造血和M1（促炎）巨噬细胞的调节。矛盾的是，PGE2抑制白细胞介素-6 （IL-6）和肿瘤坏死因子-α (TNF-α)的产生，并触发AA中脂素A4 （LXA4）的产生，从而启动炎症消退过程并增强组织再生。LXA4抑制PGE2和LTs的合成和作用，促进M2巨噬细胞生成，解决炎症。AA灭活包膜病毒，包括SARS-CoV-2。巨噬细胞、NK细胞、T细胞等免疫细胞释放AA等生物活性脂质，产生抗微生物作用。AA、PGE2和LXA4具有细胞保护作用，调节一氧化氮的产生，对维持细胞形状、控制细胞运动和吞噬、炎症、免疫和抗微生物作用至关重要。因此，我们认为AA在缺血/再灌注损伤、脓毒症、COVID-19等危重疾病的病理生物学中起着至关重要的作用，这意味着给药AA可能对这些疾病的预防和改善有显著的益处。
Arachidonic acid (AA) metabolism is critical in the initiation and resolution of inflammation. Prostaglandin E2 (PGE2) and leukotriene B4/D4/E4 (LTB4/LD4/LTE4), derived from AA, are involved in the initiation of inflammation and regulation of immune response, hematopoiesis, and M1 (pro-inflammatory) macrophage facilitation. Paradoxically, PGE2 suppresses interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) production and triggers the production of lipoxin A4 (LXA4) from AA to initiate inflammation resolution process and augment regeneration of tissues. LXA4 suppresses PGE2 and LTs’ synthesis and action and facilitates M2 macrophage generation to resolve inflammation. AA inactivates enveloped viruses including SARS-CoV-2. Macrophages, NK cells, T cells, and other immunocytes release AA and other bioactive lipids to produce their anti-microbial actions. AA, PGE2, and LXA4 have cytoprotective actions, regulate nitric oxide generation, and are critical to maintain cell shape and control cell motility and phagocytosis, and inflammation, immunity, and anti-microbial actions. Hence, it is proposed that AA plays a crucial role in the pathobiology of ischemia/reperfusion injury, sepsis, COVID-19, and other critical illnesses, implying that its (AA) administration may be of significant benefit in the prevention and amelioration of these diseases.
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影响因子：
4.3
作者：
Cho, Young Sik;Kim, Chi Hyun;Cheon, Hyae Gyeong
通讯作者：
Cheon, Hyae Gyeong
影响因子：
5.1
作者：
Chang, Cheng-Sue;Sun, Hai-Lun;Liu, Kai-Li
通讯作者：
Liu, Kai-Li
DOI：
10.1126/science.abc6261
发表时间：
2020-09-04
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Arunachalam PS;Wimmers F;Mok CKP;Perera RAPM;Scott M;Hagan T;Sigal N;Feng Y;Bristow L;Tak-Yin Tsang O;Wagh D;Coller J;Pellegrini KL;Kazmin D;Alaaeddine G;Leung WS;Chan JMC;Chik TSH;Choi CYC;Huerta C;Paine McCullough M;Lv H;Anderson E;Edupuganti S;Upadhyay AA;Bosinger SE;Maecker HT;Khatri P;Rouphael N;Peiris M;Pulendran B
通讯作者：
Pulendran B
DOI：
10.4049/jimmunol.0903816
发表时间：
2010-06-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Chan MM;Moore AR
通讯作者：
Moore AR
脂氧素 A4 通过 Nrf2 介导的气道上皮细胞中的 E-钙粘蛋白表达减轻 LPS 诱导的小鼠急性肺损伤。
影响因子：
7.4
作者：
Cheng, Xue;He, Songqing;Wu, Ping
通讯作者：
Wu, Ping