共查询到17条相似文献,搜索用时 0 毫秒
1.
Agnes Hamzaoui Anissa Berraïes Besma Hamdi Wajih Kaabachi Jamel Ammar Kamel Hamzaoui 《Immunobiology》2014
Vitamin D [25(OH)D3] deficiency has been associated with asthma as in many inflammatory and autoimmune pathologies; however, there is still a lack of data about the effects of administration of vitamin D in immune regulation in young asthmatic patients. In this study, we investigated its inhibitory effect on the immune response in young asthmatic patients and the possible mechanisms involved. 相似文献
2.
Kazunari Sugita Catherine A. Steer Itziar Martinez-Gonzalez Can Altunbulakli Hideaki Morita Francesc Castro-Giner Terufumi Kubo Paulina Wawrzyniak Beate Rückert Katsuko Sudo Susumu Nakae Kenji Matsumoto Liam OMahony Mübeccel Akdis Fumio Takei Cezmi A. Akdis 《The Journal of allergy and clinical immunology》2018,141(1):300-310.e11
3.
目的:探讨1,25-二羟维生素D3[1,25-(OH)2D3]对被动致敏人气道平滑肌细胞(HASMCs)中核因子κB(NF-κB)信号通路的影响。方法:原代培养HASMCs并使之被动致敏,以1,25-(OH)2D3作为干预因素。EMSA法检测NF-κB的DNA结合活性;免疫细胞化学染色技术观察NF-κB p65的核易位情况;Western blotting法检测核因子κB抑制蛋白α(IκBα)及p-IκBα蛋白的表达水平;实时荧光定量PCR检测维生素D受体(VDR)、维生素D 24-羟化酶(CYP24)和IκBα mRNA的表达水平;放线菌素D处理实验检测IκBα mRNA的表达。结果:(1) 1,25-(OH)2D3显著削弱被动致敏HASMCs中NF-κB的DNA结合活性及其亚单位 p65的核易位;(2) 1,25-(OH)2D3能通过增加被动致敏HASMCs中IκBα的mRNA稳定性及减少其蛋白磷酸化水平2个途径显著上调细胞中IκBα的表达;(3) 1,25-(OH)2D3显著上调被动致敏HASMCs中VDR的mRNA表达并诱发其功能性反应。结论:1,25-(OH)2D3能通过上调被动致敏HASMCs中IκBα的表达抑制细胞NF-κB信号通路,且这一作用与VDR有关,这可能是其调控被动致敏HASMCs的重要作用机制。 相似文献
4.
5.
6.
7.
8.
9.
Christos Rossios Stelios Pavlidis Uruj Hoda Chih-Hsi Kuo Coen Wiegman Kirsty Russell Kai Sun Matthew J. Loza Frederic Baribaud Andrew L. Durham Oluwaseun Ojo Rene Lutter Anthony Rowe Aruna Bansal Charles Auffray Ana Sousa Julie Corfield Ratko Djukanovic Ian M. Adcock 《The Journal of allergy and clinical immunology》2018,141(2):560-570
10.
11.
12.
13.
Eui-Baek Byun Mi-SoYang Jae-Hun Kim Du-Sup Song Byung-Soo Lee Jae-Nam Park Sang-Hyun Park Chulhwan Park Pil-Mun Jung Nak-Yun Sung Eui-Hong Byun 《Immunobiology》2014
Background
Green tea polyphenol epigallocatechin-3-gallate (EGCG) has the potential to impact a variety of inflammation-related diseases; however, the anti-inflammatory action of EGCG in endothelial cells has not been understood. Recently, we demonstrated that the 67-kDa laminin receptor (67LR) acts as a cell-surface EGCG receptor.Aim
This research was carried out to clarify the molecular basis for the down-regulation of toll-like receptor 4 (TLR4) signal transduction by EGCG in lipopolysaccharide (LPS)-stimulated endothelial cells.Results
RNAi-mediated silencing of 67LR resulted in an abrogation of the inhibitory action of EGCG on the LPS-induced activation of downstream signaling pathways. Also, we found that EGCG induced a rapid upregulation of Toll-interacting protein (Tollip), a negative regulator of TLR signaling, through 67LR in endothelial cells. RNAi-mediated silencing of Tollip impaired the TLR4 signaling inhibitory activity of EGCG. Additionally, silencing of Tollip resulted in an abrogation of the inhibitory action of EGCG on the LPS-induced expressions of cell-associated adhesion molecules, such as ICAM-1 and VCAM-1.Conclusion
Taken together, these novel findings provide new insights into an understanding of negative regulatory mechanisms of the TLR4 signaling pathway and effective therapeutic intervention for the treatment of inflammatory disease. 相似文献14.
Jae Hyon Park Dong Yeon Jeong Laurent Peyrin-Biroulet Michael Eisenhut Jae Il Shin 《Autoimmunity reviews》2017,16(1):55-63
Proinflammatory cytokines are thought to modulate pathogeneses of various inflammatory bowel diseases (IBDs). Thymic stromal lymphopoietin (TSLP), which has been studied in various allergic diseases such as asthma, atopic dermatitis (AD) and eosinophilic esophagitis (EoE), has been less considered to be involved in IBDs. However, mucosal dendritic cells (DCs) induced by various cytokines including TSLP were reported to cause polarization of T cell toward Th2 response, the differentiation of regulatory T-cell (Treg), and secretion of IgA by B cells. In this review, we discuss the concept that decreased TSLP has the potential to accelerate the development of Th1 response dominant diseases such as the Crohn's disease (CD) while increased TSLP has the potential to lead to a development of Th2 cell dominant diseases such the ulcerative colitis (UC). To examine TSLP's role as a potential determining factor for differentiating UC and CD, we analyzed the effects of other genes regulated by TSLP in regards to the UC and CD pathogeneses using data from online open access resources such as NetPath, GeneMania, and the String database. Our findings indicate that TSLP is a key mediator in the pathogenesis of IBDs and that further studies are needed to evaluate its role. 相似文献
15.
16.
17.
Xiang Meng Hao-Yue Zhou Hui-Hui Shen Eniya Lufumpa Xiao-Mei Li Biao Guo Bao-Zhu Li 《Autoimmunity reviews》2019,18(5):455-475
The role of microorganism in human diseases cannot be ignored. These microorganisms have evolved together with humans and worked together with body's mechanism to maintain immune and metabolic function. Emerging evidence shows that gut microbe and their metabolites open up new doors for the study of human response mechanism. The complexity and interdependence of these microbe-metabolite-host interactions are rapidly being elucidated. There are various changes of microbial levels in models or in patients of various autoimmune diseases (AIDs). In addition, the relevant metabolites involved in mechanism mainly include short-chain fatty acids (SCFAs), bile acids (BAs), and polysaccharide A (PSA). Meanwhile, the interaction between microbes and host genes is also a factor that must be considered. It has been demonstrated that human microbes are involved in the development of a variety of AIDs, including organ-specific AIDs and systemic AIDs. At the same time, microbes or related products can be used to remodel body's response to alleviate or cure diseases. This review summarizes the latest research of microbes and their related metabolites in AIDs. More importantly, it highlights novel and potential therapeutics, including fecal microbial transplantation, probiotics, prebiotics, and synbiotics. Nonetheless, exact mechanisms still remain elusive, and future research will focus on finding a specific strain that can act as a biomarker of an autoimmune disease. 相似文献