Molecular mechanisms of disturbed electrolyte transport in intestinal inflammation.
Diarrhea is the hallmark of both ulcerative colitis (UC) and Crohn's disease. Loss of resorptive area, destruction of epithelial cells, leaky tight junctions, and release of inflammatory mediators and products from immune cells that stimulate fluid secretion all have been implicated in the pathogenesis of inflammatory diarrhea. Very early studies in patients, however, have pinpointed the overwhelming transport abnormality in inflamed intestinal mucosa: a virtually complete loss of sodium resorptive capacity. Recently, tools have become available to study the molecular basis of disturbances in the major electrolyte transport systems during intestinal inflammation. This review gives a brief overview of the historical development of research related to electrolyte transport in inflammatory bowel disorders, focusing on the studies performed in humans, and highlights recent understanding of the molecular mechanisms that may help explain the origin of diarrhea in intestinal inflammation.
Seidler
Ursula
U
Department of Gastroenterology, Hepatology, and Endocrinology, Hannover Medical School, Hannover, Germany. seidler.ursula@mh-hannover.de
Lenzen
Henrike
H
Cinar
Ayhan
A
Tessema
Tesfaye
T
Bleich
André
A
Riederer
Brigitte
B
D001692:Biological Transport; D003424:Crohn Disease / Q000378:metabolism*; D003967:Diarrhea / Q000378:metabolism; D004573:Electrolytes / Q000378:metabolism*; D053503:Epithelial Sodium Channels; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000378:metabolism; D007408:Intestinal Absorption; D007413:Intestinal Mucosa / Q000378:metabolism*; D008954:Models, Biological; D012964:Sodium / Q000378:metabolism; D015222:Sodium Channels / Q000502:physiology
D004573:Electrolytes; D053503:Epithelial Sodium Channels; D015222:Sodium Channels; D012964:Sodium