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蝉拟青霉多糖诱导树突状细胞的表型和功能成熟。

Phenotypic and functional maturation of dendritic cells induced by polysaccharide isolated from Paecilomyces cicadae.

机构信息

College of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, Chungbuk, Korea.

出版信息

J Med Food. 2011 Jul-Aug;14(7-8):847-56. doi: 10.1089/jmf.2011.1575. Epub 2011 Jun 1.

DOI:10.1089/jmf.2011.1575
PMID:21631358
Abstract

Paecilomyces cicadae Miquel Samson is the anamorph of Cordyceps cicadae Shing and is used in functional foods for the prevention and treatment of various diseases. In the present study, we examined the effects of P. cicadae polysaccharide (PCP) on dendritic cell (DC) maturation. Phenotypic maturation of DCs by PCP was confirmed by the elevated expressions of CD80, CD86, major histocompatibility complex (MHC)-I, and MHC-II molecules and functional maturation by increased expression of interleukin-12, interleukin-1β, and tumor necrosis factor-α, enhanced allogenic T cell stimulation, and decreased endocytosis. PCP induced the maturation of DCs from C3H/HeN and C57BL/6 mice but not from Toll-like receptor (tlr) 4⁻/⁻ knockout mice and TLR4-mutated C3H/HeJ mice, which suggests that TLR4 is the membrane receptor for PCP. PCP increased the degradation of inhibitor of nuclear factor-κB (NF-κB) α/β, which enhanced the nuclear translocation of NF-κB p50/p65 and induced the phosphorylation of extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38 mitogen-activated protein kinases, which are signaling molecules downstream of TLR4. These results indicate that PCP induces DC maturation through TLR4 signaling.

摘要

蝉拟青霉(Paecilomyces cicadae Miquel Samson)是蝉拟青霉(Cordyceps cicadae Shing)的无性型,被用于预防和治疗各种疾病的功能性食品中。在本研究中,我们研究了蝉拟青霉多糖(PCP)对树突状细胞(DC)成熟的影响。通过 PCp 上调 CD80、CD86、主要组织相容性复合体(MHC)-I 和 MHC-II 分子的表达,证实了 DC 的表型成熟,通过增加白细胞介素-12、白细胞介素-1β 和肿瘤坏死因子-α 的表达、增强同种异体 T 细胞刺激和降低内吞作用,证实了 DC 的功能成熟。PCP 诱导 C3H/HeN 和 C57BL/6 小鼠的 DC 成熟,但不能诱导 TLR4⁻/⁻敲除小鼠和 TLR4 突变型 C3H/HeJ 小鼠的 DC 成熟,这表明 TLR4 是 PCP 的膜受体。PCP 增加了核因子-κB(NF-κB)α/β 的抑制剂的降解,增强了 NF-κB p50/p65 的核易位,并诱导了细胞外信号调节激酶、c-Jun N-末端激酶和 p38 丝裂原活化蛋白激酶的磷酸化,这些都是 TLR4 下游的信号分子。这些结果表明,PCP 通过 TLR4 信号诱导 DC 成熟。

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