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TREM2 表达促进感染日本血吸虫的小鼠肝脏和腹膜 M2 巨噬细胞的极化。

TREM2 expression promotes liver and peritoneal M2 macrophage polarization in mice infected with Schistosoma japonicum.

机构信息

Department of Pathogen Biology, Medical School of Nantong University, Nantong, People's Republic of China.

Department of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, People's Republic of China.

出版信息

J Cell Mol Med. 2023 Aug;27(15):2261-2269. doi: 10.1111/jcmm.17842. Epub 2023 Jul 10.


DOI:10.1111/jcmm.17842
PMID:37430471
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10399532/
Abstract

Schistosomiasis is a tropical parasitic disease that damages the liver and poses a serious threat to human health. Macrophages play a key role in the development of liver granulomas and fibrosis by undergoing polarization from M1 to M2 type during schistosomiasis. Therefore, regulating macrophage polarization is important for controlling pathological changes that occur during this disease. Triggering receptor expressed on myeloid cells 2 (TREM2) expressed on the surface of macrophages, dendritic cells and other immune cells has been shown to play a role in inhibiting inflammatory responses and regulating M2 macrophage polarization, however its role in macrophage polarization in schistosomiasis has not been investigated. In this study, we confirmed that TREM2 expression was upregulated in the livers and peritoneal macrophages of mice infected with Schistosoma japonicum. Moreover, the TREM2 expression trend correlated with the expression of M2 macrophage polarization-related molecules in the liver tissues of S. japonicum-infected mice. Using Trem2 mice, we also showed that Trem2 deletion inhibited Arg1 and Ym1 expression in liver tissues. Trem2 deletion also increased the number of F4/80 + CD86+ cells in peritoneal macrophages of infected mice. In summary, our study suggests that TREM2 may be involved in M2 macrophage polarization during schistosomiasis.

摘要

血吸虫病是一种热带寄生虫病,可损害肝脏,严重威胁人类健康。在血吸虫病中,巨噬细胞通过从 M1 向 M2 型极化,在肝肉芽肿和纤维化的发展中起关键作用。因此,调节巨噬细胞极化对于控制该疾病过程中的病理变化很重要。髓样细胞触发受体 2(TREM2)在巨噬细胞、树突状细胞和其他免疫细胞表面表达,已被证明在抑制炎症反应和调节 M2 巨噬细胞极化中发挥作用,但其在血吸虫病中巨噬细胞极化中的作用尚未得到研究。在这项研究中,我们证实 TREM2 表达在感染日本血吸虫的小鼠肝脏和腹腔巨噬细胞中上调。此外,TREM2 的表达趋势与感染日本血吸虫小鼠肝脏组织中 M2 巨噬细胞极化相关分子的表达相关。使用 Trem2 小鼠,我们还表明 Trem2 缺失抑制了肝脏组织中 Arg1 和 Ym1 的表达。Trem2 缺失还增加了感染小鼠腹腔巨噬细胞中 F4/80+CD86+细胞的数量。总之,我们的研究表明,TREM2 可能参与了血吸虫病中的 M2 巨噬细胞极化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa3/10399532/6aa22fd25bfc/JCMM-27-2261-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa3/10399532/b642fca6b4bf/JCMM-27-2261-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa3/10399532/4d3025b8db23/JCMM-27-2261-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa3/10399532/900031100c41/JCMM-27-2261-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa3/10399532/6aa22fd25bfc/JCMM-27-2261-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa3/10399532/b642fca6b4bf/JCMM-27-2261-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa3/10399532/4d3025b8db23/JCMM-27-2261-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa3/10399532/900031100c41/JCMM-27-2261-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa3/10399532/6aa22fd25bfc/JCMM-27-2261-g003.jpg

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[8]
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本文引用的文献

[1]
Switched phenotypes of macrophages during the different stages of Schistosoma japonicum infection influenced the subsequent trends of immune responses.

J Microbiol Immunol Infect. 2022-6

[2]
Insights into Macrophage/Monocyte-Endothelial Cell Crosstalk in the Liver: A Role for Trem-2.

J Clin Med. 2021-3-17

[3]
TREM-2 defends the liver against hepatocellular carcinoma through multifactorial protective mechanisms.

Gut. 2021-7

[4]
Galectins, Eosinophiles, and Macrophages May Contribute to Egg-Induced Immunopathology in a Mouse Model.

Front Immunol. 2020

[5]
TREM-2-p38 MAPK signaling regulates neuroinflammation during chronic cerebral hypoperfusion combined with diabetes mellitus.

J Neuroinflammation. 2020-1-3

[6]
Curcumin inhibits LPS-induced neuroinflammation by promoting microglial M2 polarization via TREM2/ TLR4/ NF-κB pathways in BV2 cells.

Mol Immunol. 2019-10-4

[7]
TREM-1 deficiency attenuates the inflammatory responses in LPS-induced murine endometritis.

Microb Biotechnol. 2019-7-31

[8]
Efficacy and mechanism of cGAMP to suppress Alzheimer's disease by elevating TREM2.

Brain Behav Immun. 2019-7-5

[9]
HIV and HCV augments inflammatory responses through increased TREM-1 expression and signaling in Kupffer and Myeloid cells.

PLoS Pathog. 2019-7-1

[10]
Toll-like receptor-2 regulates macrophage polarization induced by excretory-secretory antigens from Schistosoma japonicum eggs and promotes liver pathology in murine schistosomiasis.

PLoS Negl Trop Dis. 2018-12-27

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