Dysregulation of mitochondrial functions is extremely integral in the molecular pathophysiology of Crohn’s disease. These points of contact have now been shown to exist by researchers at the Technical University of Munich (TUM).
In a paper of Cell Host & Microbe, they described that defective mitochondria can cause chronic intestinal inflammation, shaping the microbiota in the mice.
While the etiologies of Crohn’s disease are still uncertain, it was originally understood several years ago that alterations in the structure and composition of the gut microbiota are linked to conditions with inflammation.
These changes are its known causes which some researchers simply cite as having caused the disease.
A team working with Dirk Haller, the chair of nutrition and immunology and the director of the Institute for Food and Health at TUM (ZIEL), has looked for the causes of these changes in the microbiome and the relationship between the microbiome and the intestinal epithelium, as well as mitochondria.
Interference with mitochondria results into changes in microbiome.
Moreover, it has been established in previous work that the intestinal epithelial cells in patients with chronic intestinal inflammation have some indicators of stress that may suggest mitochondrial dysfunction.
The researchers thus interfered with mitochondrial function in mice by stripping out a segment of the gene that codes for production of the protein Hsp60.
First, tissue damages were characterized in the Intestinal Epithelium, which looks like a Crohn’s disease. They were also identified at some levels of gene activation that are characteristic of certain stages of the disease. Moreover – a crucial shift for the question addressed by the team – microbiome reciprocated to the impaired mitochondria through the alteration in its make up.
Therefore, Dirk Haller and his team were able to provide the first evidence that mitochondrial dysfunction is indeed responsible for tissue injury in the intestines and that it also initiates pathologic alterations in the microbiome.
Prospects for new drugs
It is quite beneficial for persons with inflammatory conditions because it may possibly provide ideas for new treatments.
The big hope is to find what they call active ingredients, which would, in a sense, repair them or put them back together in the sense of fixing malfunctioning mitochondria.” This would reduce the intestinal damage as a cause of chronic low-grade inflammation processes,” states Dirk Haller.
Thus, based on our outcomes, we can assume that drugs aiming at the mitochondrial pathways or the relationships between the microbiome and mitochondria could be a significant aspect of new therapies.
Reference: Lapac A. Possible trigger of Crohn’s disease discovered: Dysfunctional mitochondria disrupt the gut microbiome
