Xu Shiping, Guo Yuxin, Luo Tiancheng, Jiang Pengfei, Yan Ziyi, He Yan, Fu Linlin, Liu Hua, Gao Zixuan, Wang Dingmin, Sun Zhengxiu, Yang Xiaoying, Pan Wei, Sun Fenfen
Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogen Biology and Immunology, Xuzhou Medical University, Xuzhou, China.
The First Clinical Medical College, Xuzhou Medical University, Xuzhou, China.
Front Vet Sci. 2022 Apr 25;9:848458. doi: 10.3389/fvets.2022.848458. eCollection 2022.
We previously reported that the larval () infection can expand the population of regulatory B cells in mice, thereby inhibiting the anti-infective immunity. However, the underlying mechanism is still largely unknown. This study further investigated the holistic transcriptomic profiles of total splenic B cells following the chronic infection of the parasite.
The infection model of larval was established by intraperitoneal inoculation with 2000 protoscolexes. Magnetic-Activated Cell Separation (MACS) was used to isolate the total splenic B cells. RNA sequencing was performed to screen the differentially expressed genes (DEGs) after infection. The expression of selected DEGs was verified using qRT-PCR. Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and Co-expression network analysis were applied to predict these DEGs' underlying biological processes, pathways, and interactions respectively.
A total of 413 DEGs were identified in larval infected B cells, including 303 up- and 110 down-regulated genes. Notably, most DEGs related to inflammation and chemotaxis were significantly upregulated after infection. In line with these changes, significant expression upregulation of DEGs associated with fatty acid oxidation, lipid synthesis, lipolysis, lipid transport, and cholesterol biosynthesis, were observed in infected B cells. Co-expression network analysis showed an intimate interaction between these DEGs associated with immune and metabolism.
The present study revealed that the larval infection induces metabolic reprogramming of B cells, which provides a novel clue to clarify the immunoregulatory mechanism of B cells in parasitic infection.
我们之前报道过，幼虫（）感染可扩大小鼠体内调节性B细胞的数量，从而抑制抗感染免疫。然而，其潜在机制仍 largely 未知。本研究进一步调查了寄生虫慢性感染后脾脏总B细胞的整体转录组概况。
通过腹腔接种2000个原头蚴建立幼虫感染模型。使用磁珠分选法分离脾脏总B细胞。进行RNA测序以筛选感染后的差异表达基因（DEG）。使用qRT-PCR验证所选DEG的表达。分别应用基因本体（GO）分析、京都基因与基因组百科全书（KEGG）通路分析和共表达网络分析来预测这些DEG潜在的生物学过程、通路和相互作用。
在幼虫感染的B细胞中总共鉴定出413个DEG，包括303个上调基因和110个下调基因。值得注意的是，大多数与炎症和趋化性相关的DEG在感染后显著上调。与这些变化一致，在感染的B细胞中观察到与脂肪酸氧化、脂质合成、脂解、脂质转运和胆固醇生物合成相关的DEG显著上调。共表达网络分析显示这些与免疫和代谢相关的DEG之间存在密切相互作用。
本研究表明，幼虫感染诱导B细胞代谢重编程，这为阐明寄生虫感染中B细胞的免疫调节机制提供了新线索。
