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免疫调节蛋白通过 TLR4-NF-κB 通路促进巨噬细胞的吞噬能力。

Immunomodulatory Protein Promotes the Phagocytic Ability of Macrophages through the TLR4-NF-κB Pathway.

机构信息

Department of Bioengineering, College of Food Science, South China Agricultural University, 483 Wushan Road, Guangzhou 510640, China.

Research Center for Micro-Ecological Agent Engineering and Technology of Guangdong Province, Guangzhou 510640, China.

出版信息

Int J Mol Sci. 2021 Nov 11;22(22):12188. doi: 10.3390/ijms222212188.

Abstract

Enhancing the phagocytosis of immune cells with medicines provides benefits to the physiological balance by removing foreign pathogens and apoptotic cells. The fungal immunomodulatory protein (FIP) possessing various immunopotentiation functions may be a good candidate for such drugs. However, the effect and mechanism of FIP on the phagocytic activity is limitedly investigated. Therefore, the present study determined effects of immunomodulatory protein (CMIMP), a novel FIP reported to induce cytokines secretion, on the phagocytosis using three different types of models, including microsphere, and . CMIMP not only significantly improved the phagocytic ability ( < 0.05), but also enhanced the bactericidal activity ( < 0.05). Meanwhile, the cell size, especially the cytoplasm size, was markedly increased by CMIMP ( < 0.01), accompanied by an increase in the F-actin expression ( < 0.001). Further experiments displayed that CMIMP-induced phagocytosis, cell size and F-actin expression were alleviated by the specific inhibitor of TLR4 ( < 0.05). Similar results were observed in the treatment with the inhibitor of the NF-κB pathway ( < 0.05). In conclusion, it could be speculated that CMIMP promoted the phagocytic ability of macrophages through increasing F-actin expression and cell size in a TLR4-NF-κB pathway dependent way.

摘要

用药物增强免疫细胞的吞噬作用,通过清除外来病原体和凋亡细胞,为生理平衡提供益处。具有多种免疫增强功能的真菌免疫调节蛋白(FIP)可能是此类药物的良好候选物。然而,FIP 对吞噬活性的影响和机制的研究还很有限。因此,本研究采用三种不同的模型,包括微球、和,确定了一种新型 FIP(CMIMP)诱导细胞因子分泌的免疫调节蛋白对吞噬作用的影响。CMIMP 不仅显著提高了吞噬能力(<0.05),而且增强了杀菌活性(<0.05)。同时,CMIMP 显著增加了细胞大小,特别是细胞质大小(<0.01),并伴随着 F-肌动蛋白表达的增加(<0.001)。进一步的实验显示,TLR4 特异性抑制剂(<0.05)可减轻 CMIMP 诱导的吞噬作用、细胞大小和 F-肌动蛋白表达。在 NF-κB 通路抑制剂的治疗中也观察到了类似的结果(<0.05)。总之,可以推测 CMIMP 通过 TLR4-NF-κB 通路依赖性增加 F-肌动蛋白表达和细胞大小来促进巨噬细胞的吞噬能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb83/8624516/3ce94dcdb779/ijms-22-12188-g001.jpg

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