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Acute pancreatitis does not result from nuclear factor κB activation in the pancreas but could inhibition of nuclear factor κB activation be of some benefit in the course of acute pancreatitis?
Acute pancreatitis is a common disease, mostly self-limiting, but in some cases an acute abdominal emergency which lacks specific therapy. Our understanding of the mechanistic processes that initiate acute pancreatitis and mediate the pathobiological responses is rapidly evolving. The discovery of mutations in the genes encoding cationic trypsinogen (PRSS1) and the pancreatic secretory trypsin inhibitor (SPINK1), which are associated with chronic pancreatitis, have supported the concept that intrapancreatic activation of digestive enzymes is a key event in the initiation of acute pancreatitis. In severe cases a systemic inflammatory response is induced resulting in multiorgan failure. Although the relationship between pancreatic injury and the uncontrolled systemic inflammatory response is unclear, several lines of evidence suggest the participation of proinflammatory cytokines, including tumour necrosis factor α (TNF-α) and interleukin (IL)-1. One key transcription factor which is activated by these proinflammatory cytokines is nuclear factor κB (NFκB). NFκB is central for the regulation of immune and inflammatory responses, proliferation, survival and tumorigenesis. The family is composed of NFκB (1 and 2) and Rel proteins (RelA, RelB and c-Rel). NFκB exists in the cytoplasm of resting cells but enters the nucleus in response to various stimuli, including proinflammatory cytokines such as TNF-α and IL-1. Activation is controlled by inhibitory subunits such as IκBα und IκBβ, which retain NFκB dimers in the cytoplasm. The IκB kinase (IKK) complex is composed of two catalytic subunits (IKK1 or α and IKK2 or β) and a regulatory subunit (IKKγ or …
Competing interests: None declared.
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