Chronic psychosocial stress has been repeatedly shown in @entity1 to be a risk factor for the development of several affective and @entity2531 , including @entity29 ( @entity29 ). There is also a large body of evidence from rodent studies indicating a link between stress and @entity344 , resembling @entity29 in @entity1 . Despite this knowledge, the detailed underlying neuroendocrine mechanisms are not sufficiently understood. This is due, in part, to a lack of appropriate animal models, as most commonly used rodent stress paradigms do not adequately resemble the @entity1 situation and/or do not cause the development of spontaneous @entity1960 . Therefore, our knowledge regarding the link between stress and @entity29 is largely based on rodent models with low face and predictive validity, investigating the effects of unnatural stressors on chemically induced @entity1960 . These studies have consistently reported that hypothalamo-pituitary-adrenal (HPA) axis activation during stressor exposure has an ameliorating effect on the severity of a chemically induced @entity1960 . However, to show the biological importance of this finding, it needs to be replicated in animal models employing more clinically relevant stressors, themselves triggering the development of spontaneous @entity1960 . Important in view of this, recent studies employing chronic/repeated psychosocial stressors were able to demonstrate that such stressors indeed cause the development of spontaneous @entity1960 and, thus, represent promising tools to uncover the mechanisms underlying stress-induced development of @entity29 . Interestingly, in these models the development of spontaneous @entity1960 was paralleled by decreased anti-inflammatory glucocorticoid (GC) signaling, whereas adrenalectomy (ADX) prior to stressor exposure prevented its development. These findings suggest a more complex role of the @entity774 in the development of spontaneous @entity1960 . In the present review I summarize the available @entity1 and rodent data in order to provide a comprehensive understanding of the biphasic role of the @entity774 and/or the GC signaling during stressor exposure in terms of spontaneous @entity1960 development.

Stress and animal models of XXXX --an update on the role of the hypothalamo-pituitary-adrenal axis.

@entity1 :: ('9606', 'Species') :: ['humans', 'human'] @entity344 :: ('MESH:D005767', 'Disease') :: ['gastrointestinal dysfunction'] @entity29 :: ('MESH:D015212', 'Disease') :: ['inflammatory bowel diseases', 'IBD'] @entity1960 :: ('MESH:D003092', 'Disease') :: ['colitis'] @entity2531 :: ('MESH:D013001', 'Disease') :: ['somatic disorders'] @entity774 :: ('MESH:D000312', 'Disease') :: ['HPA axis']
@entity29 :: (MESH:D015212,Disease) :: ['inflammatory bowel disease']
