PURPOSE Chemokines are potent regulators of the host inflammatory or immune responses. Mucosal synthesis of chemokines may be important in the pathogenesis of mucosal inflammation in ulcerative colitis (UC). We performed this study to investigate the expression of C-X-C chemokine genes in UC. METHODS Mucosal tissues were obtained from six normal controls and six UC patients by endoscopic biopsies. In patients with UC, mucosal tissues were separately obtained from both involved and uninvolved regions. RNA was extracted and mRNA levels of five C-X-C chemokines were determined by quantitative reverse transcription-PCR using internal RNA standards. RESULTS Mucosal mRNA levels of all chemokines tested increased in the involved region of UC compared with the uninvolved region of UC or normal controls. CONCLUSION Our data suggest that mucosal expression of C-X-C chemokines contributes to the pathogenesis of UC
Shim, Ki Nam , Yang, Suk Kyun , Myung, Seung Jae , Kim, Ok Hee , Oh, Hyun Ju , Lee, Jeong A , Cho, Yoon Kyung , Yu, Chang Sik , Jung, Hwoon Yong , Hong, Weon Seon , Kim, Jin Ho , Min, Young Il
PURPOSE To better understand the extent to which chemokines participate in the mucosal inflammatory response in patients with ulcerative colitis (UC), we assessed the expression of an array of chemokines in the colonic mucosa of UC patients. METHODS Colonic mucosal biopsy specimens were obtained from 15 patients with UC and 12 normal controls. Messenger RNA (mRNA) levels for 10 chemokines were quantitated by reverse-transcription PCR using synthetic standard RNAs. The biopsy specimens were also cultured, and secreted chemokines in culture supernatants were assayed by ELISA. RESULTS The mRNA expression of C-X-C (IL-8, GROalpha, GRObeta, GROgamma, ENA-78, and IP-10) and C-C (MCP-1, MIP-1beta, and RANTES), but not C (lymphotactin) chemokines was significantly higher in the affected mucosa of UC patients than in the unaffected mucosa of UC patients or in the normal mucosa of normal controls. The degree of increased expression was more prominent in the C-X-C than in the C-C chemokines. Further, the secretion of IL-8, GROalpha, ENA-78, and MCP-1 was higher in UC patients than in normal controls. Secretions of MIP-1beta and RANTES also showed a trend toward an increase in UC, but it did not reach statistical significance. CONCLUSION The increased expression of a variety of chemokines in UC suggest that chemokines may play an important role in the immunopathogenesis of UC.