Although there has been progress in understanding the pathogenesis of IBD in the last decade, the etiology remains unknown. Therefore, most therapies aim at a symptomatic treatment of inflammation. However, objective assessment of mucosal inflammation and disease activity is often difficult. Neither CAI nor EAI, as established scores, can characterize mucosal inflammation and disease activity to the full extent. The CAI is influenced by patients' perception and may thus reflect clinical symptoms due to other factors than mucosal inflammation and the severity of endoscopic lesions often do not correlate with clinical severity.
The aim of our study was to find a simple and objective means to quantify inflammatory activity in colonic mucosa of UC patients. Therefore, we tried to establish several biomarkers, which can reflect mucosal inflammation in UC.
Thus, we measured the transcript levels of CXCL8, CXCL10, calgranulin B and CXCL2 in biopsies of UC patients and correlated them to CAI and EAI.
The new and substantial finding of our study is the significant positive correlation between transcript levels of CXCL8, CXCL10, calgranulin B and CXCL2 and both CAI and EAI.
Our results agree with the literature. For CXCL8, which is the major attractant and activator of neutrophils [9, 10, 16], a high expression of mRNA in UC patients with high disease activity has been described . Another group , who performed immunohistochemistry and image analysis found enhanced CXCL10 expression in UC. CXCL10 selectively attracts activated T lymphocytes. Calgranulin B is selectively secreted by human monocytes and granulocytes. Using ELISA technique an increased serum level was detected in UC patients with active disease . The same group  could also show a greater calgranulin B production in CD in ulcerative and fissural lesions than in uninflamed areas. Concerning CXCL2, which is extremely chemotactic for neutrophils , an upregulated expression of mRNA and protein in inflamed gut, predominantly in UC has been shown .
These data from the literature strengthen our findings that CXCL8, CXCL10, calgranulin B and CXCL2 are objective indicators of disease activity and severity in UC.