Key result
Patients with Crohn's disease had significantly lower LC3-II expression in mesenteric tissue and higher LC3-II, TNF-α, and IL-23 in intestinal mucosa compared to controls (p < 0.05).
Case-Control (n=26)
p-value: p=<0.05
Crohn's disease is associated with a defect in autophagic activity in creeping fat tissue, which may contribute to maintaining intestinal inflammation.
Impaired mesenteric autophagy may sustain Crohn's inflammation but should not change practice; hypothesis-generating for targeted therapies.
Background Recently, mesenteric fat has been proposed to play a role in the pathophysiol- ogy of Crohn's disease (CD), as fat hypertrophy is detected close to the affected intestinal area; however, there are few studies regarding autophagy and creeping fat tissue in CD. Objective Evaluate autophagy-related proteins and proinflammatory cytokines in intestinal mucosa and mesenteric fat in patients with CD and controls. Patients and methods Ten patients with CD, eight with non-inflammatory disease who underwent surgery, and eight with normal ileocolonoscopy were studied. The expression of LC3-II, TNF-α and IL-23 was determined by immunoblot of protein extracts. In addition, total RNA of LC3 and Atg16-L1 were determined using RT-PCR. Results The expression of LC3-II was significantly lower in the mesenteric tissue of CD when compared to controls (p < 0.05). In contrast, the intestinal mucosa of the CD group had higher levels of LC3-II (p < 0.05). However, mRNA expression of autophagy-related pro- teins was similar when compared to mesenteric fat groups. TNF-α and IL-23 expressions were higher in intestinal mucosa of CD than in control (p < 0.05). Conclusion These findings suggest a defect in the autophagic activity of the creeping fat tissue in CD, which could be involved with the maintenance of the inflammatory process in the intestinal mucosa.
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Leal et al. (2013) conducted a case-control in Crohn's disease (n=26). Crohn's disease vs. Controls (non-inflammatory disease or normal ileocolonoscopy) was evaluated on Expression of LC3-II, TNF-α and IL-23 in intestinal mucosa and mesenteric fat (p=<0.05). Patients with Crohn's disease had significantly lower LC3-II expression in mesenteric tissue and higher LC3-II, TNF-α, and IL-23 in intestinal mucosa compared to controls (p < 0.05).
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