scholarly journals Baicalin Inhibits IL-17-Mediated Joint Inflammation in Murine Adjuvant-Induced Arthritis

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Xue Yang ◽  
Ji Yang ◽  
Hejian Zou
Keyword(s):  
Rheumatoid Arthritis ◽  
Adhesion Molecule ◽  
Th17 Cells ◽  
Chinese Herb ◽  
Population Expansion ◽  
Joint Inflammation ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Necrosis Factor Alpha ◽  
Adjuvant Induced Arthritis

T-helper-17 (Th17) cells are implicated in a number of inflammatory disorders including rheumatoid arthritis. Antagonism of Th17 cells is a treatment option for arthritis. Here, we report that Baicalin, a compound isolated from the Chinese herb Huangqin (Scutellaria baicalensisGeorgi), relieved ankle swelling and protected the joint against inflammatory destruction in a murine adjuvant-induced arthritis model. Baicalin inhibited splenic Th17 cell population expansionin vivo. Baicalin prevented interleukin- (IL-) 17-mediated lymphocyte adhesion to cultured synoviocytes. Baicalin also blocked IL-17-induced intercellular adhesion molecule 1, vascular cell adhesion molecule 1, IL-6, and tumor necrosis factor-alpha mRNA expression in cultured synoviocytes. Collectively, these findings suggest that Baicalin downregulates the joint inflammation caused by IL-17, which is likely produced by an expanded population of splenic Th17 cells in experimental arthritis. Baicalin might be a promising novel therapeutic agent for treating rheumatoid arthritis in humans.

scholarly journals Amnion-derived cells express intercellular adhesion molecule-1: regulation by cytokines

1999 ◽  
Vol 22 (2) ◽  
pp. 193-205 ◽  
Author(s):  
KW Marvin ◽  
WR Hansen ◽  
HC Miller ◽  
RL Eykholt ◽  
MD Mitchell
Keyword(s):  
Adhesion Molecule ◽  
Present Report ◽  
Cellular Protein ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Tnf Alpha ◽  
Protein Synthesis Inhibitor ◽  
Intercellular Adhesion Molecule 1 ◽  
Synthesis Inhibitor ◽  
Necrosis Factor Alpha

We have examined the expression of the intercellular adhesion molecule-1 (ICAM-1) mRNA in primary and established amnion-derived cell cultures and regulation of this expression by tumour necrosis factor-alpha (TNF-alpha) and interleukin (IL)-1beta. TNF-alpha (50 ng/ml) and IL-1beta (1.0 ng/ml) induced 18- and 11-fold increases respectively in expression of the ICAM-1 mRNA in WISH cells (an amnion epithelium-derived cell line). The increase was detectable within one hour of treatment and peaked by two hours. The protein synthesis inhibitor, cycloheximide (10 microg/ml) did not inhibit this induction. Increased levels of ICAM-1 protein were detected in the cells within 4 h after initiation of treatment with either cytokine. By 16 h of treatment with IL-1beta or TNF-alpha ICAM-1 reached 40 and 73 pg/microg cellular protein, representing 6- and 11-fold stimulations respectively. In primary amnion cells, basal expression of ICAM-1 mRNA was undetectable. However, TNF-alpha (50 ng/ml) induced ICAM-1 mRNA within two hours, peak expression being reached between four and eight hours after initiation of treatment. The present report demonstrates for the first time that amnion derived cells can express ICAM-1 and, further, that this expression is regulated by pro-inflammatory cytokines. This has implications for the amnion as a possible source for soluble ICAM-1, for this gene product as a marker for preterm labour, and for participation of the amnion, additional to its reported secretory role, in inflammatory processes of the fetal membranes.

scholarly journals KRIT1 Deficiency Promotes Aortic Endothelial Dysfunction

2019 ◽  
Vol 20 (19) ◽  
pp. 4930 ◽  
Author(s):  
Francesco Vieceli Dalla Sega ◽  
Raffaella Mastrocola ◽  
Giorgio Aquila ◽  
Francesca Fortini ◽  
Claudia Fornelli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Adhesion Molecule ◽  
Umbilical Vein ◽  
Intercellular Adhesion Molecule ◽  
Loss Of Function ◽  
Intercellular Adhesion Molecule 1 ◽  
Necrosis Factor Alpha ◽  
Aortic Endothelial

Loss-of-function mutations of the gene encoding Krev interaction trapped protein 1 (KRIT1) are associated with the pathogenesis of Cerebral Cavernous Malformation (CCM), a major cerebrovascular disease characterized by abnormally enlarged and leaky capillaries and affecting 0.5% of the human population. However, growing evidence demonstrates that KRIT1 is implicated in the modulation of major redox-sensitive signaling pathways and mechanisms involved in adaptive responses to oxidative stress and inflammation, suggesting that its loss-of-function mutations may have pathological effects not limited to CCM disease. The aim of this study was to address whether KRIT1 loss-of-function predisposes to the development of pathological conditions associated with enhanced endothelial cell susceptibility to oxidative stress and inflammation, such as arterial endothelial dysfunction (ED) and atherosclerosis. Silencing of KRIT1 in human aortic endothelial cells (HAECs), coronary artery endothelial cells (HCAECs), and umbilical vein endothelial cells (HUVECs) resulted in increased expression of endothelial proinflammatory adhesion molecules vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) and in enhanced susceptibility to tumor necrosis factor alpha (TNF-α)-induced apoptosis. These effects were associated with a downregulation of Notch1 activation that could be rescued by antioxidant treatment, suggesting that they are consequent to altered intracellular redox homeostasis induced by KRIT1 loss-of-function. Furthermore, analysis of the aorta of heterozygous KRIT1+/− mice fed a high-fructose diet to induce systemic oxidative stress and inflammation demonstrated a 1.6-fold increased expression of VCAM-1 and an approximately 2-fold enhanced fat accumulation (7.5% vs 3.6%) in atherosclerosis-prone regions, including the aortic arch and aortic root, as compared to corresponding wild-type littermates. In conclusion, we found that KRIT1 deficiency promotes ED, suggesting that, besides CCM, KRIT1 may be implicated in genetic susceptibility to the development of atherosclerotic lesions.

scholarly journals Increased levels of circulating intercellular adhesion molecule 1 in the sera of patients with rheumatoid arthritis

1993 ◽  
Vol 36 (8) ◽  
pp. 1098-1102 ◽  
Author(s):  
John J. Cush ◽  
Robert Rothlein ◽  
Herbert B. Lindsley ◽  
Elizabeth A. Mainolfi ◽  
Peter E. Lipsky
Keyword(s):  
Rheumatoid Arthritis ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1

Treatment of refractory rheumatoid arthritis with a monoclonal antibody to intercellular adhesion molecule 1

1994 ◽  
Vol 37 (7) ◽  
pp. 992-999 ◽  
Author(s):  
Arthur F. Kavanaugh ◽  
Laurie S. Davis ◽  
Lisa A. Nichols ◽  
Stephen H. Norris ◽  
Robert Rothlein ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Monoclonal Antibody ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Refractory Rheumatoid Arthritis
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