期刊
FRONTIERS IN IMMUNOLOGY
卷 13, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2022.999945
关键词
refined polysaccharide from Dendrobium devonianum (DVP-1); immune regulation; TLR4/MyD88/NF-?B pathway; H1N1 influenza virus; prevent infection
类别
资金
- Zhejiang Provincial Science and Technology Council [LGF21H280008]
- National Natural Science Foundation of China [82174050]
- Project of Hangzhou Medical College [YS2021015]
- Huadong Medicine Joint Funds of the Zhejiang Provincial Natural Science Foundation of China [LHDMZ22H300009]
- Zhejiang Provincial Medicinal Health Program [2020PY005, 2021KY130]
- Project of Educational Commission of Zhejiang Province [Y202045371]
- Project of Administration of Traditional Chinese Medicine of Zhejiang Province [2022ZB221]
The novel polysaccharide DVP-1 from Dendrobium devonianum activates immunity through the TLR4/MyD88/NF-kappa B pathway, which enhances the ability of mice to prevent H1N1 influenza virus infection.
Dendrobium polysaccharide exhibits multiple biological activities, such as immune regulation, antioxidation, and antitumor. However, its resistance to viral infection by stimulating immunity is rarely reported. In this study, we explored the effect and mechanism of DVP-1, a novel polysaccharide from Dendrobium devonianum, in the activation of immunity. After being activated by DVP-1, the ability of mice to prevent H1N1 influenza virus infection was investigated. Results of immune regulation showed that DVP-1 significantly improved the immune organ index, lymphocyte proliferation, and mRNA expression level of cytokines, such as IL-1 beta, IL-4, IL-6, and TNF-alpha in the spleen. Immunohistochemical results showed that DVP-1 obviously promoted the mucosal immunity in the jejunum tissue. In addition, the expression levels of TLR4, MyD88, and TRAF6 and the phosphorylation levels of TAK1, Erk, JNK, and NF-kappa B in the spleen were upregulated by DVP-1. The virus infection results showed that the weight loss of mice slowed down, the survival rate increased, the organ index of the lung reduced, and the virus content in the lung decreased after DVP-1 activated immunity. By activating immunity with DVP-1, the production of inflammatory cells and inflammatory factors in BALF, and alveolar as well as peribronchiolar inflammation could be prevented. The results manifested that DVP-1 could resist H1N1 influenza virus infection by activating immunity through the TLR4/MyD88/NF-kappa B pathway.
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