<i>Cordyceps militaris</i> Immunomodulatory Protein Promotes the Phagocytic Ability of Macrophages through the TLR4-NF-κB Pathway
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 e...
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| Autores principales: | , , , , , , |
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| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
MDPI AG
2021
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/e41a1149ec664745b6f1b5db3522ecd3 |
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| Sumario: | 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 <i>Cordyceps militaris</i> immunomodulatory protein (CMIMP), a novel FIP reported to induce cytokines secretion, on the phagocytosis using three different types of models, including microsphere, <i>Escherichia Coli</i> and <i>Candida albicans</i>. CMIMP not only significantly improved the phagocytic ability (<i>p</i> < 0.05), but also enhanced the bactericidal activity (<i>p</i> < 0.05). Meanwhile, the cell size, especially the cytoplasm size, was markedly increased by CMIMP (<i>p</i> < 0.01), accompanied by an increase in the F-actin expression (<i>p</i> < 0.001). Further experiments displayed that CMIMP-induced phagocytosis, cell size and F-actin expression were alleviated by the specific inhibitor of TLR4 (<i>p</i> < 0.05). Similar results were observed in the treatment with the inhibitor of the NF-κB pathway (<i>p</i> < 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. |
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