COMMENTARY

Inflammatory bowel disease

The complicated path to true causes of disease: role of nuclear factor B in inflammatory bowel disease

S Schreiber

Correspondence to:
Correspondence to:
Professor S Schreiber
Hospital for General Internal Medicine and Institute for Clinical Molecular Biology, Christian-Albrechts-University, Schittenhelmstrasse 12, 24105 Kiel, Germany; s.schreiber@mucosa.de

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Challenging our understanding of the role of nuclear factor B activation in the pathophysiology of intestinal inflammation in human inflammatory bowel disease

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Keywords: collagenous colitis; inflammatory bowel disease; nitric oxide synthase; nuclear factor B; ulcerative colitis; Crohn’s disease

The first 150 words of the full text of this article appear below.

Nuclear factor kappa B (NFB) was discovered as a transcription factor some 15 years ago.¹ Since then the protein has been linked to early pathophysiological events in a host of inflammatory conditions. NFB, in most instances, is a heterodimer composed of a p50 and p65 subunit. In most mammalian cells NFB is found in the resting state in the cytoplasm where it is bound in a complex to a protein that is a member of a family of specific inhibitors (IKK). Following phosphorylation, the inhibitor is rapidly degraded and the released NFB migrates within minutes into the nucleus where it can specifically induce gene expression by binding to sequence defined DNA elements in gene promoter regions.

Even after more than a decade of mechanistic and clinical studies, the role of NFB in intestinal inflammation is not fully understood as its activity as . . . [Full text of this article]

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