Background: NF-kappaB regulates a large number of genes involved in the inflammatory response to critical illness, but it is not well known if and how NF-kappaB is activated in the gut following traumatic brain injury (TBI) and what is the role of cytokine-mediated inflammation in the pathogenesis of acute gut mucosal injury.
Materials and methods: Male Wistar rats were randomly divided into control and TBI groups, each of which was subgrouped at hours 3, 12, 24, and 72 and on day 7. Parietal brain contusion was produced by a free-falling weight on the exposed dura of the right parietal lobe. NF-kappaB binding activity in jejunal tissue was measured using EMSA and the concentrations of TNF-alpha and IL-6 were detected using ELISA.
Results: NF-kappaB binding activity in the jejunum was significantly increased at 3 h following TBI, was maximal at 72 h, and remained elevated by 7 days postinjury. TNF-alpha and IL-6 concentrations were also significantly increased by 3 h postinjury, but peaked at 24 h and remained elevated on Day 7 postinjury.
Conclusions: TBI induced a rapid and persistent up-regulation of NF-kappaB and proinflammatory cytokines in the gut, which may play an important role in the pathogenesis of acute gut mucosal injury mediated by inflammation.