Research: Inflammatory Mediator Regulates Diarrhea In Inflammatory Bowel Disease
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Inflammatory Mediator Regulates Diarrhea In Inflammatory Bowel Disease
04 Jan 2010
Researchers led by Dr. Terrence A. Barrett of Northwestern University
Medical School in Chicago. Illinois have discovered that activation of
NK-κB, an inflammatory mediator, results in diarrhea in inflammatory
bowel disease (IBD). These results are presented in the January 2010
issue of the American Journal of Pathology.
IBD, which affects approximately 1 in 500 people in the United States,
describes a group of diseases, including Crohn's disease and
ulcerative colitis, with inflammation in the intestinal tract.
Patients with IBD experience diverse symptoms, including abdominal
pain, vomiting, diarrhea, bloody stools, and weight loss.
Immune responses contribute to mucosal permeability, and hence
diarrhea, in IBD; however, the mechanisms that govern this response
are not completely understood. Tang et al therefore examined the role
of NK-κB, an inflammatory mediator, in IBD-induced diarrhea. Following
immune activation, blocking NK-κB expression in the cells lining the
intestinal tract inhibited diarrhea and prevented protein changes in
these cells, resulting in decreased leakiness between the cells. These
findings suggest that immune cell-mediated activation of NK-κB in IBD
promotes the movement of fluid into the bowel lumen, resulting in
diarrhea.
Tang et al suggest that "NK-κB activation opens paracellular spaces
and promotes movement of fluid into bowel lumen. ... Importantly,
changes in permeability were associated with a net movement of water
and solute into the bowel lumen. These data not only correlated with
clinical signs of diarrhea but also help explain the initial fluid
accumulation observed in previous studies."
Tang Y, Clayburgh DR, Mittal N, Goretsky T, Dirisina R, Zhang Z, Kron
M, Ivancic D, Katzman RB, Grimm G, Lee G, Fryer J, Nusrat A, Turner
JR, Barrett TA: Epithelial NK-κB enhances transmucosal fluid movement
by altering tight junction protein composition after T cell
activation. Am J Pathol 2010, 176: 158-167
Source: Dr. Angela Colmone
American Journal of Pathology
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Luke