Format

Send to

Choose Destination
Dev Comp Immunol. 2017 Aug;73:21-26. doi: 10.1016/j.dci.2017.03.002. Epub 2017 Mar 2.

Echinacea pupurea extracts promote murine dendritic cell maturation by activation of JNK, p38 MAPK and NF-κB pathways.

Author information

1
Key Laboratory of Molecular Animal Nutrition and Feed Sciences, College of Animal Science, Zhejiang University, Hangzhou, 310058, PR China; Animal Nutrition and Human Health Laboratory, School of Life Sciences, Hunan Normal University, Changsha, 410006, PR China.
2
Key Laboratory of Molecular Animal Nutrition and Feed Sciences, College of Animal Science, Zhejiang University, Hangzhou, 310058, PR China.
3
International Medical Center, Zhejiang Provincial People's Hospital, Hangzhou, 310014, PR China.
4
Qilu Animal Health Products Co., Ltd., Jinan, 250100, PR China.
5
Key Laboratory of Molecular Animal Nutrition and Feed Sciences, College of Animal Science, Zhejiang University, Hangzhou, 310058, PR China. Electronic address: weifenli@zju.edu.cn.
6
Key Laboratory of Molecular Animal Nutrition and Feed Sciences, College of Animal Science, Zhejiang University, Hangzhou, 310058, PR China. Electronic address: xuxg@zju.edu.cn.

Abstract

Dendritic cells (DCs) comprise a system of highly professional antigen presenting cells (APCs) which connect innate and adaptive immunity by undergoing dramatic shift in their maturation state. Phytomedicine Echinacea purpurea extracts (EE) could modulate murine dendritic cell fate and function. However, the underlying mechanism of EE on DCs development and maturation remains limited. In this study, immature DCs were induced phenotypic maturation with up-regulated expression of key accessory molecules and the phagocytic activity was decreased after being treated with EE (400 μg/ml) for 48 h. We found that TLR1/2, JNK, p38-MAPK and NF-κB pathways were activated following EE exposure. Notably, JNK activation was demonstrated to be associated with increased IFN-γ response while p38-MAPK pathway exhibited immuno-regulatory effects via induction of IL-10 and TGF-β1. Furthermore, it was verified that NF-κB signaling was responsible for EE-induced synthesis of IFN-γ, IL-12 and TGF-β1, but not for IL-10 induction. These results indicate that EE have the immunomodulatory potency to promote both phenotypic and functional maturation of BMDCs via modulating the activation of JNK, p38-MAPK and NF-κB pathways. Our findings contributed to the current understanding of the immunoregulatory function of EE and the mechanism of DCs maturation.

KEYWORDS:

Dendritic cells; E. purpurea; MAPKs; Maturation; NF-κB; TLRs

PMID:
28263837
DOI:
10.1016/j.dci.2017.03.002
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center