摘要：
血吸虫病主要由虫卵沉积于肝肠组织引起免疫病理性疾病。虫卵的分泌物和排泄物都可以作为抗原物质，通过多种机制刺激巨噬细胞、树突状细胞、中性粒细胞、T细胞和调节性B细胞（regulatory B cell, Breg细胞）等分泌细胞因子和趋化因子，从而刺激宿主的免疫应答，影响虫卵肉芽肿和纤维化的发生、发展。有些虫卵抗原可以诱导M2型巨噬细胞、2型辅助性T细胞（type 2 helper T cell, Th2细胞）、调节性T细胞（regulatory T cell, Treg细胞）和Breg细胞的分化，可以用于某些炎症疾病和免疫疾病的治疗。现主要对虫卵抗原诱导免疫细胞的机制和作用作一概述。
作者机构：
[梁瑜; 刘彦; 邹冬雪; 彭莉; 高勇强; 胡丽; 刘俊] Institute of Pathogenic Biology, Hengyang Medical School, University of South China, Hengyang 421001, China;[肖建华] Institute of Pathogenic Biology, Hengyang Medical School, University of South China, Hengyang 421001, China. *Corresponding author, E-mail: jhxiao223@163.com
摘要：
Aims & ScopeFoundations of Chemistry is an international journal which seeks to provide an interdisciplinary forum where chemists, biochemists, philosophers, historians, educators and sociologists with an interest in foundational issues can discuss conceptual and fundamental issues which relate to the `central science' of chemistry. Such issues include the autonomous role of chemistry between physics and biology and the question of the reduction of chemistry to quantum mechanics. The journal will publish peer-reviewed academic articles on a wide range of subdisciplines, among others: chemical models, chemical language, metaphors, and theoretical terms; chemical evolution and artificial self-replication; industrial application, environmental concern, and the social and ethical aspects of chemistry's professionalism; the nature of modeling and the role of instrumentation in chemistry; institutional studies and the nature of explanation in the chemical sciences; theoretical chemistry, molecular structure and chaos; the issue of realism; molecular biology, bio-inorganic chemistry; historical studies on ancient chemistry, medieval chemistry and alchemy; philosophical and historical articles; and material of a didactic nature relating to all topics in the chemical sciences. Foundations of Chemistry plans to feature special issues devoted to particular themes, and will contain book reviews and discussion notes. Audience: chemists, biochemists, philosophers, historians, chemical educators, sociologists, and other scientists with an interest in the foundational issues of science.Coverage in the Journals@Ovid database begins with the March 1999 issue.
期刊：
International Journal of Clinical and Experimental Medicine,2019年12(2):1535-1544 ISSN：1940-5901
通讯作者：
Xiao, Jianhua
作者机构：
[Li, Lifang; Xiao, Jianhua] Univ South China, Hengyang Med Coll, Inst Pathogen Biol, 28 Changsheng Rd, Hengyang 421001, Peoples R China.;[Li, Lifang; Zou, Yan; Yan, Dewen; Lin, Guangfeng; Zhang, Tingji] Second Peoples Hosp Shenzhen, Shenzhen 518037, Peoples R China.
通讯机构：
[Xiao, Jianhua] U;Univ South China, Hengyang Med Coll, Inst Pathogen Biol, 28 Changsheng Rd, Hengyang 421001, Peoples R China.
关键词：
Type 2 diabetes mellitus;Baihu decoction;adipose tissue;chronic inflammation;CD14
摘要：
The incidence of Type 2 diabetes mellitus (T2DM) has increased worldwide. This study investigated the effect of a herbal extract, named as Baihu decoction (BHD), in treating T2DM by using mouse adipose cells and a mouse T2DM model. Mouse 3T3-L1 preadipocytes were cultured in DMEM culture medium and used for experiments when about 90% fat-differentiated cells were mature. The KM male mouse diabetes model was established by injecting streptozotocin. Thirty two KM T2DM mice were randomly divided into 4 groups, with 8 mice in each group. Enzyme-linked immunosorbent assays (ELISA) and Reverse Transcription-quantitative PCR (RT-real time-PCR) were performed to investigate the levels of inflammatory factors and adipokines related to diabetes and their mRNA levels. Western blot experiments were carried out to determine levels of a series of proteins. BHD reduced inflammatory responses induced by lipopolysaccharide in mouse adipose cells and repressed the activity of the CD14/TLR4-NF-kappa B signal pathway. Our siRNA experimental results demonstrated that decreased CD14 gene expression reduced the levels of inflammation significantly. The animal experimental results indicated that BHD has an effective effect on reduction of blood sugar level of T2DM mice. Furthermore, this anti-diabetic effect was due to inhibition of the activity of the CD14/TLR4-NF-kappa B signal pathway, especially CD14. BHD has anti-diabetic effect both in vitro and in vivo by down-regulating the activity of the CD14/TLR4-NF-kappa B signaling pathway, especially CD14.
摘要：
Objective: Zymosan A is a type of fungus polysaccharide that is derived from the cell wall of yeast and induces immune responses associated with fungal infection. In this study, our aim was to observe the expression and degradation of the following cytokines: TNF-alpha, CXCL1, IL-10 and IL-23a. These cytokines were induced by Zymosan A via primary peritoneal macrophages (pM Phi s), and they had more AU-rich elements (ARE) within their 3'-UTR mRNA sequence. Additionally, we would like to explore the mechanism underlying the p38 regulation of the ARE-mRNA stability of the related cytokines in the MAPK signaling pathway. Methods: Primary peritoneal macrophages (pM Phi s) were isolated and purified from C57 mice and stimulated with Zymosan A. The mRNA expressions of TNF-alpha, CXCL1, IL-10 and IL-23a that were induced by Zymosan A were detected by Real-time PCR, and the mRNA 3'-UTR sequences of these cytokines were analyzed using bio-informatic methods. The activation of MAPK signaling pathways and blocking experiments in pM Phi s treated with Zymosan A were identified by western blot, and the change in TTP, which is a type of RNA binding protein, was observed through in vitro enzymatic activity experiments. Results: Zymosan A induces a high expression of TNF-alpha, CXCL1, IL-10 and IL-23a and activates the MAPK signaling pathway through the phosphorylation of p38, ERK, and JNK and the RNA binding protein TTP. Bio-informatic analysis showed that the mRNA 3' UTR region of the related cytokines contained numerous AU-rich element (ARE) sequences. In the MAPK signaling pathway activated by Zymosan A, the ERK inhibitor PD98059 and the JNK inhibitor SP600125 had no effect on the ARE-mRNA stability of these cytokines. Conversely, the p38 inhibitor SB202190 effectively inhibited the phosphorylation of the downstream MK2 and TTP within the p38 signaling pathway and quickly degraded the mRNA of the above cytokines. An in vitro enzymatic activity experiment also proved that the phosphorylation of TTP disappeared after the treatment of lambda PP, which is a type of phosphoesterase. Conclusions: Zymosan A induces the high expression of TNF-alpha, CXCL1, IL-10 and IL-23a, which contain ARE-mRNA, and effectively activates MAPK signaling pathways through the phosphorylation of p38, ERK and JNK. In MAPK signaling pathways, p38 plays an important role about the mRNA stability and can enhance the ARE-mRNA stability of the above cytokines, the mechanism of its effect may be that p38 phosphorylate the downstream MK2 and TTP, which leads to the phosphorylated TTP can't combine with the mRNA ARE sequence and degrades the mRNA effectively.
