In addition, other stress-modulated mechanisms, such as altered secretion of chemokines and neuropeptides other than CRH (e.g. neurotensin, and substance P, vasoactive intestinal peptide), as well as activation of immune, or other origin cell subsets, may further confer to neuro–immune crosstalk, resulting in disturbance of intestinal cytokine balance and barrier integrity during the course of IBD progression [67,68]. Here, CRH is linked to irritable bowel syndrome.