The Inflammatory Tissue Microenvironment in IBD

被引:43
作者
Colgan, Sean P. [1 ]
Curtis, Valerie F. [1 ]
Campbell, Eric L. [1 ]
机构
[1] Univ Colorado, Div Gastroenterol, Mucosal Inflammat Program, Aurora, CO 80045 USA
基金
美国国家卫生研究院;
关键词
mucosa; inflammation; colitis; neutrophil; epithelium; hypoxia; resolution; HYPOXIA-INDUCIBLE FACTOR; NF-KAPPA-B; FACTOR-I; EXPERIMENTAL COLITIS; BOWEL-DISEASE; ADENOSINE RECEPTORS; DEPENDENT INDUCTION; MUCOSAL INFLAMMATION; INTESTINAL EPITHELIA; ENERGY-METABOLISM;
D O I
10.1097/MIB.0b013e31828dcaaf
中图分类号
R57 [消化系及腹部疾病];
学科分类号
100201 [内科学];
摘要
A current view of the inflammatory bowel diseases (IBDs) includes the luminal triggering of innate immune disease in a genetically susceptible host. Given the unique anatomy and complex environment of the intestine, local microenvironmental cues likely contribute significantly to both disease progression and resolution in IBD. Compartmentalized tissue and microbe populations within the intestine result in significant metabolic shifts within these tissue microenvironments. During active inflammatory disease, metabolic demands often exceed supply, resulting in localized areas of metabolic stress and diminished oxygen delivery (hypoxia). There is much recent interest in harnessing these microenvironmental changes to the benefit of the tissue, including targeting these pathways for therapy of IBD. Here, we review the current understanding of metabolic microenvironments within the intestine in IBD, with discussion of the advantages and disadvantages of targeting these pathways to treat patients with IBD.
引用
收藏
页码:2238 / 2244
页数:7
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