期刊
PEDIATRICS INTERNATIONAL
卷 56, 期 6, 页码 873-883出版社
WILEY
DOI: 10.1111/ped.12362
关键词
CXCR3 axis components; inflammatory bowel disease; microarray; matrix metalloproteinase families; reverse transcription polymerase chain reaction
类别
资金
- Grants-in-Aid for Scientific Research [24591585] Funding Source: KAKEN
BackgroundAlthough pediatric inflammatory bowel disease (IBD) is characterized by extensive intestinal involvement and rapid early progression, the precise cause and specific factors involved in disease aggravation have not been well established. The aim of this study was to investigate the pathogenesis of pediatric IBD. MethodsThe expression of inflammatory molecules in colon samples taken from active ulcerative colitis (UC) and Crohn's disease (CD) patients was compared with those of controls. Three children each with UC and CD in both the active and remission phase and their controls were enrolled, and the inflammatory gene expression in the mucosa was examined by microarray. Additionally, six children from each group were further enrolled in a real-time reverse transcription polymerase chain reaction and an immunohistochemical study to examine the expression of CXCL9, 10, 11, CXCR3, matrix metalloproteinase (MMP)-1, -3, -7, and -10. ResultsThe microarray analysis revealed enhanced expression of the CXCL9, 10, and 11 genes in the active phase of CD. The expression of MMP-1, -3, -7, and -10 was significantly enhanced in the active phase of UC. These changes were also confirmed by real-time reverse transcription polymerase chain reaction. Immunohistochemical analysis revealed enhanced expression of CXCL9, 10, and 11 in both the lamina propria and epithelial cells in these patients. CXCR3-positive cells were also confirmed in the lamina propria. The expression of MMP-1, -3, -7, and -10 was also enhanced in the mucosal epithelial cells and the lamina propria in both CD and UC patients. ConclusionsThese findings suggest that CXCR3 axis components and MMP play an important role in the mucosal damage in pediatric IBD.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据