核心岩藻糖基化缺失抑制了鼠伤寒沙门氏菌感染小鼠的体液免疫反应。
Loss of core fucosylation suppressed the humoral immune response in Salmonella typhimurium infected mice.
机构信息
College of Basic Medical Science, Dalian Medical University, 9-Western Section, Lvshun South Road, Dalian, Liaoning, 116044, China.
Division of Regulatory Glycobiology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, Miyagi, Japan.
出版信息
J Microbiol Immunol Infect. 2021 Aug;54(4):606-615. doi: 10.1016/j.jmii.2020.02.006. Epub 2020 Feb 21.
BACKGROUND
The humoral immune response is pivotal to protect the host from Salmonella typhimurium (S. typhimurium) infection. Previously, we found that core fucosylation catalyzed by core fucosyltransferase (Fut8) could regulate the immune responses. However, the role of core fucosylation during S. typhimurium infection remains unclear.
METHODS
To demonstrate the role of Fut8 in S. typhimurium infection, we infected Fut8 and Fut8 mice using S. typhimurium. The production of antiserum against the S. typhimurium was detected. The expression of T and B cell activation-related genes during S. typhimurium infection was analyzed. The role of core fucosylation on CD4 T-B cell interaction and B cell generation was investigated during S. typhimurium infection. The production of sIgA was compared between Fut8 and Fut8 mice.
RESULTS
Compared to Fut8 mice, the number of S. typhimurium colonized in the cecum was markedly increased in Fut8 mice. The production of the IgG and sIgA specific for S. typhimurium was significantly decreased in Fut8 mice. Moreover, loss of Fut8 decreased the induction of Th2-type cytokines from splenic cells of Fut8 mice during S. typhimurium infection. In addition, we found that the core fucosylation regulated the interaction between B and T cells in the lipid raft formation.
CONCLUSION
Core fucosylation plays important roles in host defence against S. typhimurium infection.
背景
体液免疫反应对于宿主抵抗沙门氏菌（Salmonella typhimurium，S. typhimurium）感染至关重要。先前，我们发现核心岩藻糖基化（core fucosylation）由核心岩藻糖基转移酶（core fucosyltransferase，Fut8）催化，可调节免疫反应。然而，核心岩藻糖基化在 S. typhimurium 感染过程中的作用尚不清楚。
方法
为了证明 Fut8 在 S. typhimurium 感染过程中的作用，我们使用 S. typhimurium 感染 Fut8 和 Fut8 小鼠。检测针对 S. typhimurium 的抗血清产生情况。分析 S. typhimurium 感染过程中 T 和 B 细胞激活相关基因的表达。研究 S. typhimurium 感染过程中核心岩藻糖基化对 CD4 T-B 细胞相互作用和 B 细胞生成的作用。比较 Fut8 和 Fut8 小鼠之间 sIgA 的产生情况。
结果
与 Fut8 小鼠相比，Fut8 小鼠盲肠中 S. typhimurium 的定植数量明显增加。Fut8 小鼠针对 S. typhimurium 的 IgG 和 sIgA 产生显著减少。此外，Fut8 缺失降低了 Fut8 小鼠脾细胞在 S. typhimurium 感染过程中 Th2 型细胞因子的诱导。此外，我们发现核心岩藻糖基化调节了 B 和 T 细胞在脂质筏形成中的相互作用。
结论
核心岩藻糖基化在宿主抵抗 S. typhimurium 感染中发挥重要作用。
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