Our investigation of the various UPR-related molecules at the protein levels correlated relatively well the results obtained by qRT-PCR, which is a technique far more sensitive. But the correlation is not perfect and this could be caused by a combination of factors: restricted biopsy samples in immunoblotting, lower sensitivity of this technique, and induction of ER stress by the biopsy technique itself, as it is reported in other tissues . Nonetheless, we Abmole CPI-613 consider that the global picture strengthens the findings made by qRT-PCR. An expanded qPCR analysis of 16 UPR-related genes confirmed that a higher basal UPR activity is in place in the ileal mucosa of healthy controls when compared to the colonic mucosa. In this analysis, twelve genes had significantly higher transcript levels in samples of ileal controls than in colonic controls, clearly showing that the two tissues live with a different basal activation of the UPR. A growing body of evidence suggests that ER stress and inflammation are interconnected. HSPA5 is a reliable marker for ER stress and IL8 is a marker for inflammation. We found a strong correlation between these two in both UC and colonic CD, but a lack of correlation was found in ileal CD. This is coherent with the increased UPR activation observed in the colonic tissue of active IBD patients, whereas no increase was seen in the ileal tissue of active CD patients. In the ileum, ER stress is probably dictated by other local factors. The ileum contains a high number of Paneth cells, has an increased number of mucosa-associated E. coli and has a higher metabolic activity compared to the colon. This might contribute to a constitutive triggering of the UPR in the ileal mucosa, which is critical in maintaining homeostasis. The fact that inflammation does not further increase UPR in ileal samples Dabrafenib citations either reflects that the higher basal levels observed can buffer some perturbations or reflect that the ileum is less sensitive to perturbations through inflammation. This leads us to consider that the colonic mucosa is subject to a lower ER stress, with a significant increase in inflammatory conditions: from low basal levels of UPR, any induction is more uniform and more noticeable in this tissue. In order to determine whether the ileum could still respond to ER stress, paired colonic and ileal samples of five healthy controls were stimulated with tunicamycin, a well-known ER stress inducer . Both colonic and ileal samples revealed higher HSPA5 transcript levels in the tunicamycin stimulated samples.