Table of Contents Author Guidelines Submit a Manuscript
Canadian Journal of Gastroenterology
Volume 17 (2003), Issue 1, Pages 31-36
Original Article

Role of Na+/H+ Exchanger Isoform-1 in Human Inflammatory Bowel Disease

Islam Khan,1 Iqbal Siddique,2,3 Farida M Al-Awadi,1 and Krishna Mohan3

1Department of Biochemistry, Faculty of Medicine, Kuwait University, Kuwait
2Department of Medicine, Faculty of Medicine, Kuwait University, Kuwait
3Thuniyan Al-Ghanim Gastroenterology Center, Al-Amiri Hospital, Kuwait

Copyright © 2003 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


BACKGROUND: Na+/H+ exchanger (NHE) is responsible for a net uptake of sodium chloride and water from the gastrointestinal tract and maintains electrolyte and water homeostasis. However, its status in human inflammatory bowel disease such as ulcerative colitis (UC) and Crohn’s disease (CD) remains poorly understood.

OBJECTIVES: To investigate the role of NHE-1 isoform in human CD and UC.

METHODS: Expression of NHE-1 protein and messenger ribonucleic acid and sodium pump activity were examined in the colonic biopsy samples taken from UC (n=11) and CD (n=13) patients using enhanced chemiluminescence-Western blot analysis, reverse transcription polymerase chain reaction and spectrophotometry. Subjects presenting with abdominal pain and endoscopically normal colon served as normal controls (n=11). Myeloperoxidase (MPO) activity and histology were performed to confirm tissue inflammation.

RESULTS: MPO activity increased significantly (P<0.05) in both UC and CD patients compared with the normal controls. Parallel to MPO activity profile, there was also a significantly higher infiltration of inflammatory cells in both cases. P-nitrophenylphosphatase activity, a marker of the sodium pump, remained unchanged in CD but increased significantly (P<0.05) in UC compared with the normal controls. On the contrary, the level of NHE-1 protein and messenger ribonucleic acid was significantly decreased (P<0.05) in both cases, whereas the internal control, a-actin remained unaltered.

CONCLUSIONS: These findings demonstrate a transcriptionally regulated suppression of NHE-1 in both UC and CD. This NHE-1 suppression may reduce an uptake of sodium chloride and water from the inflamed colonic lumen and thus contribute to diarrhea and neuromuscular alterations in these conditions.