4.7 Article

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

Journal

Publisher

MDPI
DOI: 10.3390/ijms222212188

Keywords

Cordyceps militaris; immunomodulatory protein; macrophage; phagocytosis; immunity

Funding

  1. State Key Research and Development Plan Modern Food Processing, Food Storage and Transportation Technology and Equipment [2017YFD0400204-03, 2018YED0401200]
  2. National Natural Science Foundation of China [31572178, 31772373, 31601564]

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CMIMP significantly enhanced the phagocytic ability of immune cells and increased bactericidal activity through increasing F-actin expression and cell size in a TLR4-NF-kappa B pathway dependent way.
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 Cordyceps militaris immunomodulatory protein (CMIMP), a novel FIP reported to induce cytokines secretion, on the phagocytosis using three different types of models, including microsphere, Escherichia Colt and Candida albicans. CMIMP not only significantly improved the phagocytic ability (p < 0.05), but also enhanced the bactericidal activity (p < 0.05). Meanwhile, the cell size, especially the cytoplasm size, was markedly increased by CMIMP (p < 0.01), accompanied by an increase in the F-actin expression (p < 0.001). Further experiments displayed that CMIMP-induced phagocytosis, cell size and F-actin expression were alleviated by the specific inhibitor of TLR4 (p < 0.05). Similar results were observed in the treatment with the inhibitor of the NF-kappa B pathway (p < 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-kappa B pathway dependent way.

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