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巨噬细胞清道夫受体CD163在介导宿主细胞感染中的作用评估。

Assessment of the Macrophage Scavenger Receptor CD163 in Mediating Infection of Host Cells.

作者信息

Deng Xiangwei, Li Shuilian, Zhu Ying, Yu Bo, Zhang Jing, Fang Qianhai, Li Zhimin, Chen Hongbo, Zhou Huanhuan

机构信息

Laboratory of Genetic Breeding, Reproduction and Precision Livestock Farming & Hubei Provincial Center of Technology Innovation for Domestic Animal Breeding, School of Animal Science and Nutritional Engineering, Wuhan Polytechnic University, Wuhan 430023, China.

出版信息

Vet Sci. 2023 Mar 21;10(3):235. doi: 10.3390/vetsci10030235.

Abstract

The macrophage CD163 surface glycoprotein is a member of the SRCR family class B, which has been identified as the key trigger in host-pathogen interactions, but its specific roles in sensing () infection are largely unknown. Here, we investigated porcine CD163 in mediating the adhesion and immune response of using in vitro host-bacteria interaction models. CD163-overexpressing Chinese hamster ovary K1 cells (CHO-K1) showed obvious subcellular localization in the cytoplasm, especially in the cytomembrane. Although detection using scanning electron microscopy (SEM) confirmed the bacterial adhesion, there was no significant difference in the adhesion of to CHO-K1 cells between the presence and absence of CD163. In addition, similar results were observed in 3D4/21 cells. Meanwhile, bindings of to nine synthetic peptides, the bacterial binding motifs within SRCR domains of CD163, were weak based on a solid-phase adhesion assay and agglutination assay. Moreover, CD163 had no effect on the expression of -induced inflammatory cytokines (IL-6, INF-γ, IL-10, IL-4 and TGF-β) in CHO-K1 cells. In conclusion, these findings indicate that porcine CD163 plays a minor role in sensing infection.

摘要

巨噬细胞CD163表面糖蛋白是B类SRCR家族的成员,已被确定为宿主-病原体相互作用中的关键触发因素,但其在感知()感染中的具体作用尚不清楚。在此,我们使用体外宿主-细菌相互作用模型研究了猪CD163在介导()的黏附及免疫反应中的作用。过表达CD163的中国仓鼠卵巢K1细胞(CHO-K1)在细胞质中呈现明显的亚细胞定位,尤其是在细胞膜中。尽管使用扫描电子显微镜(SEM)检测证实了细菌黏附,但有无CD163时()对CHO-K1细胞的黏附并无显著差异。此外,在3D4/21细胞中也观察到了类似结果。同时,基于固相黏附试验和凝集试验,()与CD163的SRCR结构域内的九个合成肽(细菌结合基序)的结合较弱。此外,CD163对()诱导的CHO-K1细胞中炎性细胞因子(IL-6、INF-γ、IL-10、IL-4和TGF-β)的表达没有影响。总之,这些发现表明猪CD163在感知()感染中起次要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b660/10054613/c4bee85e482a/vetsci-10-00235-g001.jpg

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