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Psychological stress in IBD: new insights into pathogenic and therapeutic implications

机译:IBD中的心理压力:致病和治疗意义的新见解

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Psychological stress has long been reported anecdotally to increase disease activity in inflammatory bowel disease (IBD), and recent well designed studies have confirmed that adverse life events, chronic stress, and depression increase the likelihood of relapse in patients with quiescent IBD. This evidence is increasingly supported by studies of experimental stress in animal models of colitis. With the evolving concept of psychoneuroimmunology, the mechanisms by which the nervous system can affect immune function at both systemic and gut mucosal levels are gradually becoming apparent. Recent data suggest that stress induced alterations in gastrointestinal inflammation may be mediated through changes in hypothalamic-pituitaryadrenal(HPA) axis function and alterations in bacterial-mucosal interactions, and via mucosal mast cells and mediators such as corticotrophin releasing factor (CRF). To date, the therapeutic opportunities offered by stress reduction therapy remain largely unexplored, in part becauseof methodological difficulties of such studies. This paper reviews recent advances in our understanding of the pathogenic role of psychological stress in IBD and emphasises the need for controlled studies of the therapeutic potential of stress reduction.
机译:长期以来,一直有人报道过心理压力会增加炎症性肠病(IBD)的疾病活动,而最近经过精心设计的研究证实,不良的生活事件,慢性压力和抑郁症会增加IBD静态患者复发的可能性。结肠炎动物模型中的实验压力研究越来越多地支持这一证据。随着神经神经免疫学概念的发展,神经系统在全身和肠道粘膜水平上影响免疫功能的机制逐渐变得明显。最新数据表明,应激诱导的胃肠道炎症改变可能是通过下丘脑-垂体-肾上腺(HPA)轴功能的变化和细菌-粘膜相互作用的改变,以及通过粘膜肥大细胞和诸如促肾上腺皮质激素释放因子(CRF)的介导的。迄今为止,减轻压力疗法所提供的治疗机会仍未得到充分探索,部分原因是此类研究的方法学困难。本文回顾了我们对IBD中心理应激的致病作用的理解的最新进展,并强调需要对减轻应激的治疗潜力进行对照研究。

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