NF-kB is the Master Switch in inflammatory bowel disease – it’s chronically turned on in Crohn’s and ulcerative colitis

Chronic inflammation in the gut primarily defines Crohn’s disease and ulcerative colitis. That inflammation results from excess activation of NF-kB, which itself probably results from the combination of a body that has excess inflammation to begin with, plus environmental factors, plus genetic vulnerability.

Inhibiting NF-kB could be very helpful in the fight against inflammatory bowel disease.

The publication:

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J Intern Med. 2008 Jun;263(6):591-6.

NF-kappaB in inflammatory bowel disease.

Atreya I, Atreya R, Neurath MF.

Summary of the abstract

Apart from genetic and environmental factors, the mucosal immune system of the gut plays a central role in the pathogenesis of inflammatory bowel disease (IBD).

In the healthy gut, the mucosal immune system ensures the balance between pro- and anti-inflammatory mediators and thereby allows an effective defence against luminal pathogens while preventing an overwhelming immune reaction.

In Crohn’s disease and ulcerative colitis this immunological balance is severely impaired and shifted towards the pro-inflammatory side.

The chronic mucosal inflammation in IBD is caused by hyperactivation of immune cells, which produce high levels of pro-inflammatory cytokines like TNF, IL-6 and interferon-gamma, resulting in colonic tissue damage.

The nuclear transcription factor kappaB (NF-kB) was identified as one of the key regulators in this immunological setting. Its activation is markedly induced in IBD patients and through its ability to promote the expression of various pro-inflammatory genes, NF-kB strongly influences the course of mucosal inflammation.

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