基质金属蛋白酶
肠道通透性
医学
失调
肠道菌群
冲程(发动机)
炎症
免疫学
细胞外基质
缺血性中风
缺血
细胞生物学
生物
内科学
机械工程
工程类
作者
Jonathan Larochelle,Changjun Yang,Lei Liu,Eduardo Candelario‐Jalil
出处
期刊:Stroke
[Lippincott Williams & Wilkins]
日期:2022-07-29
卷期号:53 (10): 3238-3242
被引量:8
标识
DOI:10.1161/strokeaha.122.040144
摘要
Poststroke infections are common complications of stroke and are highly associated with poor outcomes for patients. Stroke induces profound immunodepression coupled with alterations to autonomic signaling, which together render the body more susceptible to infection from without (nosocomial/community-acquired infection) and from within (commensal bacterial infection). Critical to the hypothesis of commensal infection is the phenomenon of poststroke gut permeability and gut dysbiosis. Few studies have provided adequate explanations for the mechanisms underlying the molecular alterations that produce a more permeable gut and perturbed gut microbiota after stroke. A dysregulation in the production of matrix MMP-7 (metalloproteinase-7) may play a critical role in the progression of gut permeability after stroke. By cleaving junctional and extracellular matrix proteins, MMP-7 is capable of compromising gut barrier integrity. Because of MMP-7’s unique abundance in the small intestine and its capacity to be induced in states of bacterial invasion and inflammation, along with its unique degradative capability, MMP-7 may be crucially important to the progression of gut permeability after ischemic stroke.
科研通智能强力驱动
Strongly Powered by AbleSci AI