Chen Shenghong, Xie Yaochen, Guo Dingqian, Li Tiansen, Tan Zhen, Ran Xuhua, Wen Xiaobo
Hainan Key Lab of Tropical Animal Reproduction and Breeding and Epidemic Disease Research, Department of Animal Science and Technology, School of Tropical Agriculture and Forestry (School of Agricultural and Rural Affairs, School of Rural Revitalization), Hainan University, Haikou, China.
Front Microbiol. 2025 Jan 24;16:1514115. doi: 10.3389/fmicb.2025.1514115. eCollection 2025.
infections can lead to intestinal inflammation and metabolic disorders in birds. However, whether arachidonic acid (ARA) metabolism is involved in -induced intestinal inflammation remains unclear. This experiment investigated the changes in cecal flora and ARA metabolism in Hainan Wenchang chickens infected with using 16s rDNA sequencing and targeted metabolomics. The results showed that the levels of ARA metabolites were increased in the cecum tissue of Wenchang chickens after infection with , including prostaglandin E2 (PGE), prostaglandin F2α (PGF), lipoxin A4 (LXA4), ± 8(9)-EET, ± 11(12)-EET, and ± 8,9-DiHETrE. The content of key enzymes for ARA production and metabolism (Phospholipase A2 PLA2 and Cyclooxygenase-2 COX-2) in chicken cecum tissues was increased after infection. The relative mRNA levels of inflammatory factors were also increased after infection, including Interferon-γ (IFN-γ), Transforming growth factor-β1 (TGF-β1), Interleukin-4 (IL-4), and Interleukin-6 (IL-6). In HD11 cells, the use of a cyclooxygenase (COX) inhibitor reduced the increased levels of COX-2 and PGF induced by infection and effectively reduced the inflammatory response. In addition, the number of beneficial genera (e.g., , , and ) in the cecum of Wenchang chickens was significantly reduced after infection with . The present study revealed the structure of cecal flora in -infected Wenchang chickens. In addition, this study demonstrated that activates the ARA cyclooxygenase metabolic pathway, which in turn mediates the development of intestinal inflammation in Wenchang chickens. The results can provide data support and theoretical support for the prevention and control of avian salmonellosis.
感染可导致禽类肠道炎症和代谢紊乱。然而,花生四烯酸(ARA)代谢是否参与[具体感染因素未提及]诱导的肠道炎症仍不清楚。本实验采用16S rDNA测序和靶向代谢组学方法,研究了感染[具体感染因素未提及]的海南文昌鸡盲肠菌群和ARA代谢的变化。结果表明,感染[具体感染因素未提及]后,文昌鸡盲肠组织中ARA代谢产物水平升高,包括前列腺素E2(PGE)、前列腺素F2α(PGF)、脂氧素A4(LXA4)、±8(9)-环氧二十碳三烯酸(±8(9)-EET)、±11(12)-环氧二十碳三烯酸(±11(12)-EET)和±8,9-二羟二十碳四烯酸(±8,9-DiHETrE)。感染[具体感染因素未提及]后,鸡盲肠组织中ARA产生和代谢的关键酶(磷脂酶A2 PLA2和环氧化酶-2 COX-2)含量增加。感染后炎症因子的相对mRNA水平也升高,包括干扰素-γ(IFN-γ)、转化生长因子-β1(TGF-β1)、白细胞介素-4(IL-4)和白细胞介素-6(IL-6)。在HD11细胞中,使用环氧化酶(COX)抑制剂可降低感染[具体感染因素未提及]诱导的COX-2和PGF水平升高,并有效减轻炎症反应。此外,感染[具体感染因素未提及]后,文昌鸡盲肠中有益菌属(如[具体有益菌属未提及]、[具体有益菌属未提及]和[具体有益菌属未提及])的数量显著减少。本研究揭示了感染[具体感染因素未提及]的文昌鸡盲肠菌群结构。此外,本研究表明[具体感染因素未提及]激活了ARA环氧化酶代谢途径,进而介导文昌鸡肠道炎症的发展。研究结果可为禽沙门氏菌病的防控提供数据支持和理论支持。