Indeed, whereas in UC patients a continuous inflammation with a sharp delineation between the involved and non-involved mucosa is seen, inflammation in CD patients is characterized by the presence of endoscopically noninvolved mucosa between affected regions, known as ��skip�� lesions. No increase in IL8 expression was observed in samples taken in the non-inflamed mucosa of Abmole Company PCI-32765 active UC patients, while in the noninflamed mucosa of active CD patients a significant increase in IL8 was found. A ROC curve analysis including or excluding noninflamed samples of active CD patients confirmed that the inclusion of those non-inflamed samples cause a decrease of almost 30% in sensitivity for IL8. In conclusion our results show that the use of endoscopically non-inflamed samples of active CD patients does not represent an appropriate control for the study of molecular inflammation. We first investigated UPR activation by HSPA5 expression. HSPA5, also known as GRP78 or BiP, is a central player in ER homeostasis. Under homeostatic conditions, the luminal domain of the proximal sensors ATF6, IRE1 and PERK1 interacts with HSPA5, inactivating these signaling INCB28060 customer reviews pathways. Upon accumulation of unfolded or misfolded proteins, HSPA5 dissociates from these molecules, allowing their activation . The transcriptional activation of the HSPA5 promoter is regarded as a reliable measure of ER stress . Literature reports increased HSPA5 mRNA levels in colonic and ileal samples of involved areas of IBD patients. In line with these data, our results demonstrated significant increased HSPA5 transcript and/ or protein levels in involved areas of colonic IBD patients. In contrast to the study of Kaser, we found no differential expression of HSPA5 between ileal samples of healthy controls and active CD patients . However, we suspect that this could be due to the use of a limited sample size in the study of Kaser, along with an important variability in the expression of ileal HSPA5 protein . Nonetheless, our data reflects well activation of the UPR as not only HSPA5 was modulated, but also other transcript and/or protein levels: PDIA4, XBP1s and pEIF2A. These were found to be increased in colonic IBD, while no differential expression of both transcript and protein levels were observed in ileal CD. In this context, we are confident that our results reflect fairly the situation given the reasonable number of biological replicates, the analysis of multiple UPR-related genes and the correlation between transcript and protein levels in our work.