Cytokines in the colon, central nervous system and serum of irritable bowel syndrome rats

Objective: The aim of this study was to detect the expression of interleukin (IL)-1 beta and transforming growth factor (TGF)-beta 1 in the colonic tissue and serum of irritable bowel syndrome (IBS) rats, as well as the distribution and expression of corticotropin-releasing factor (CRF) in the spinal cord and brain of the visceral hypersensitivity rats, thus to ascertain the mechanism of visceral hypersensitivity signal conduction pathway. Methods: The expression of IL-1 beta and TGF-beta 1 in the colonic tissue and serum of IBS rats was screened by the liquid chip technology and verified by RT-PCR technology. Then the quantitative analysis of CRF in the spinal cord and brain was achieved by the immunohistochemical method and computerized image system. Result: The rat model with visceral hypersensitivity was successfully established. Among the screened indicators of IL-1 beta and TGF-beta 1 in colon tissue and serum, only the expression of IL-1 beta in the model group was up-regulated (P < 0.05). The immunohistochemical method showed that CRF was expressed in the spinal cord, hypothalamus, and the third ventricle. The positive index number of the model groups was higher than that of the control group (P < 0.01). Conclusion: From the research, it can be inferred that IL-1 beta may participate in the pathogenesis mechanism of IBS via regulating the colon function. The increasing expression of CRF linked to stress in the spinal cord, hypothalamus and the third ventricle indicated that it might play an important role in the mechanisms of visceral hypersensitivity signal conduction pathway.

Automated summary

This study aimed to investigate the expression of interleukin (IL)-1 beta and transforming growth factor (TGF)-beta 1 in the colonic tissue and serum of irritable bowel syndrome (IBS) rats, as well as the distribution and expression of corticotropin-releasing factor (CRF) in the spinal cord and brain of the visceral hypersensitivity rats. The findings suggest that IL-1 beta may participate in the pathogenesis mechanism of IBS, while the increased expression of CRF in the spinal cord, hypothalamus, and third ventricle may play a significant role in the mechanisms of visceral hypersensitivity signal conduction pathway.