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类志贺邻单胞菌感染诱导了锯齿鳗(Mastacembelus armatus)肝胰腺中的铁死亡和凋亡。

Plesiomonas shigelloides infection induced ferroptosis and apoptosis in hepatopancreas of zig-zag eel (Mastacembelus armatus).

作者信息

Yu Zhide, Yin Xiaoli, Zhu Wenshi, Chen Yiman, Zhang Li'nan, Shu Hu

机构信息

School of Life Sciences, Guangzhou University, Guangzhou, 511400, PR China.

School of Life Sciences, Guangzhou University, Guangzhou, 511400, PR China; College of Light Chemical Industry and Materials Engineering, Shunde Polytechnic, Foshan, 528333, PR China.

出版信息

Fish Shellfish Immunol. 2025 Nov;166:110681. doi: 10.1016/j.fsi.2025.110681. Epub 2025 Aug 31.

Abstract

The zig-zag eel (Mastacembelus armatus) is a commercially important fish species in southern China, yet its susceptibility to Plesiomonas shigelloides (P. shigelloides) infection remains poorly understood. In this study, 100 μL of YY001 (1 × 10 CFU/mL) was used to intraperitoneally infect the zig-zag eel, and its effect on the hepatopancreas of the M. armatus was observed. The histopathology analysis of hepatopancreas revealed hemorrhage, tissue loosening, enlarged intercellular spaces, and increased cellular vacuolation. Transcriptomic profiling identified 5508 differentially expressed genes (DEGs), with significant enrichment in immune and metabolic pathways, especially in ferroptosis and apoptosis pathways, and these genes were upregulated in the infection group. Subsequently, we confirmed these findings through biochemical assays, TUNEL staining and qPCR. The results showed that GPX activity in hepatopancreas of M. armatus was significantly decreased, and iron ion (Fe) concentration and malondialdehyde (MDA) were significantly increased after infection. Furthermore, the results of gpx4 and scl7a11 genes expression in hepatopancreas of the M. armatus was significantly downregulated after infection, while the expression of ferroptosis marker genes lpcat3 and ncoa4 was significantly up-regulated. These results indicate that ferroptosis occurred in the hepatopancreas cells of the M. armatus after infection with P. shigelloides. The results of TUNEL staining showed that after infection with P. shigelloides, apoptosis occurred in the hepatopancreatic cells of the zig-zag eel, and the expressions of the apoptosis genes casp3, casp8, and bax genes were significantly upregulated, while the expression of the apoptosis inhibitor gene bcl2 was significantly downregulated. These results all indicate that P. shigelloides infection can cause ferroptosis and apoptosis in the hepatopancreas of the zig-zag eel, leading to hepatopancreatic lesions. Our study provides new insights into the pathogenesis of fish diseases caused by P. shigelloides.

摘要

锯齿鳗(Mastacembelus armatus)是中国南方一种具有重要商业价值的鱼类,但人们对其感染类志贺邻单胞菌(Plesiomonas shigelloides,简称P. shigelloides)的易感性仍知之甚少。在本研究中,用100 μL的YY001(1×10 CFU/mL)对锯齿鳗进行腹腔注射感染,并观察其对锯齿鳗肝胰腺的影响。肝胰腺的组织病理学分析显示有出血、组织疏松、细胞间隙增大和细胞空泡化增加。转录组分析鉴定出5508个差异表达基因(DEGs),在免疫和代谢途径中显著富集,尤其是在铁死亡和凋亡途径中,且这些基因在感染组中上调。随后,我们通过生化分析、TUNEL染色和qPCR证实了这些发现。结果表明,感染后锯齿鳗肝胰腺中的GPX活性显著降低,铁离子(Fe)浓度和丙二醛(MDA)显著增加。此外,感染后锯齿鳗肝胰腺中gpx4和scl7a11基因的表达显著下调,而铁死亡标记基因lpcat3和ncoa4的表达显著上调。这些结果表明,感染P. shigelloides后,锯齿鳗肝胰腺细胞发生了铁死亡。TUNEL染色结果显示,感染P. shigelloides后,锯齿鳗肝胰腺细胞发生凋亡,凋亡基因casp3、casp8和bax基因的表达显著上调,而凋亡抑制基因bcl2的表达显著下调。这些结果均表明,P. shigelloides感染可导致锯齿鳗肝胰腺发生铁死亡和凋亡,进而导致肝胰腺病变。我们的研究为P. shigelloides引起的鱼类疾病发病机制提供了新的见解。

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