Inflammatory cells' role in acetic acid-induced colitis.

BACKGROUND: FREE RADICALS ARE THE KNOWN MECHANISMS RESPONSIBLE FOR INDUCING COLITIS WITH TWO ORIGINS: Inflammatory cells and tissues. Only the inflammatory cells can be controlled by corticosteroids. Our aim was to assess the importance of neutrophils as one of the inflammatory cells in inducing colitis and to evaluate the efficacy of corticosteroids in the treatment of inflammatory bowel disease (IBD). MATERIALS AND METHODS: Thirty-six mice were divided into six groups of six mice each. Colitis was induced in three groups by exposing them to acetic acid through enema (group 1), ex vivo (group 3), and enema after immune suppression (group 5). Each group had one control group that was exposed to water injection instead of acetic acid. Tissue samples were evaluated and compared based on macroscopic damages and biochemical and pathological results. RESULTS: Considering neutrophilic infiltration, there were significant differences between groups 1, 3, 5, and the control of group 1. Groups 3, 5, and their controls, and group 1 and the control of group 3 had significant differences in terms of goblet depletion. Based on tissue originated H2O2, we found significant differences between group 1 and its control and group 3, and also between groups 5 and the control of group 3. All the three groups were significantly different from their controls based on Ferric Reducing Ability of Plasma (FRAP) and such differences were also seen between group 1 with two other groups. CONCLUSION: Neutrophils may not be the only cause of oxidation process in colitis, and also makes the effectiveness of corticosteroids in the treatment of this disease doubtful.

Cell cycle analysis of the CD133(+) and CD133(-) cells isolated from human colorectal cancer.

AIM: The CD133 antigen has been identified as a putative stem cell marker in colorectal cancer tissues. The aim of this study was to investigate the cell cycle state of CD133(+) and CD133(-) cells, isolated from primary human colorectal tumors. MATERIALS AND METHODS: After mechanical and enzymatic dissociation of the tumor samples, CD133(+) and CD133(-) subsets were identified and separated by magnetic cell sorting. Flow cytometric analysis was performed to compare the cell cycle of both CD133(+) and CD133(-) cells isolated from primary and liver metastatic cancer cells. RESULTS: The results indicated that CD133(+) cells isolated from both primary and liver metastatic colorectal cancers were found in higher percentage in the G0/G1 phases. However, the CD133(-) cells isolated from primary colorectal cancers were predominantly found in the S and G2/M phases. Surprisingly, the CD133(-) cells isolated from liver metastatic colorectal cancers were mostly found in the G0/G1 phase. CONCLUSION: The present study provides evidence that CD133(+) cells are in a quiescent state in colorectal cancer, representing a mechanism that would at least partially explain chemotherapy resistance and tumor recurrence in post-therapy patients.