Mitochondrial dysfunction in inflammatory bowel disease

Abstract

Inflammatory Bowel Disease (IBD) represents a group of idiopathic disorders characterized by chronic or recurring inflammation of the gastrointestinal tract. While the exact etiology of disease is unknown, IBD is recognized to be a complex, multifactorial disease that results from an intricate interplay of genetic predisposition, an altered immune response, changes in the intestinal microbiota, and environmental factors. Together, these contribute to a destruction of the intestinal epithelial barrier, increased gut permeability, and an influx of immune cells. Given that most cellular functions as well as maintenance of the epithelial barrier is energy-dependent, it is logical to assume that mitochondrial dysfunction may play a key role in both the onset and recurrence of disease. Indeed several studies have demonstrated evidence of mitochondrial stress and alterations in mitochondrial function within the intestinal epithelium of patients with IBD and mice undergoing experimental colitis. Although the hallmarks of mitochondrial dysfunction, including oxidative stress and impaired ATP production are known to be evident in the intestines of patients with IBD, it is as yet unclear whether these processes occur as a cause of consequence of disease. We provide a current review of mitochondrial function in the setting of intestinal inflammation during IBD.

Geniposide ameliorates TNBS-induced experimental colitis in rats via reducing inflammatory cytokine release and restoring impaired intestinal barrier function

“…Damaged intestinal epithelial barrier function is correlated with triggering or worsening intestinal inflammatory disorder [42] . Both maintenance and disruption of epithelial barrier function are related to intestinal inflammation.…”

Mitochondria and redox balance in coeliac disease: A case‐control study

“…Present findings confirm the existence of elevated concentrations of inflammation-associated molecules in patients with CD. 2,3 Specifically, while the pleiotropic IL-6 cytokine concentrations were not different between patients and HC, the significantly higher IL-8 circulating concentrations in patients endorsed the specific role played by IL-8 in mediating the pro-inflammatory response in the GI tract 18 and the mucosal damage. 32 Also IL-1b circulating concentrations were significantly higher in patients with CD than in HC.…”

Protective Actions of Epithelial 5-Hydroxytryptamine 4 Receptors in Normal and Inflamed Colon

“…2627 Therefore, Caco-2 cells were exposed to the free radical donor, H 2 O 2 (200 μM), and cell survival in response to 5-HT 4 receptor stimulation was determined using the SRB assay. H 2 O 2 caused a significant reduction in cell survival compared to untreated cells (Fig.…”