New Research Links Mitochondrial Dysfunction to Crohn’s Disease, Offering Hope for Targeted Treatments

New Research Links Mitochondrial Dysfunction to Crohn’s Disease, Offering Hope for Targeted Treatments

(IN BRIEF) Researchers at the Technical University of Munich have found that mitochondrial dysfunction in the intestines can trigger Crohn’s disease symptoms by disrupting the gut microbiome. This groundbreaking discovery establishes a direct link between defective mitochondria and both tissue damage and microbiome changes. The research offers promising new directions for treatments that could target mitochondrial function to reduce inflammation in patients with Crohn’s disease.

(PRESS RELEASE) MUNICH, 11-Oct-2024 — /EuropaWire/ — Researchers at the Technical University of Munich (TUM) have uncovered a significant link between dysfunctional mitochondria and the onset of Crohn’s disease. The team, led by Professor Dirk Haller, demonstrated that defective mitochondrial function in mice leads to symptoms of chronic intestinal inflammation and alters the gut microbiome, offering new insights into the disease’s potential triggers.

Mitochondria, known as the energy powerhouses of cells, are vital for cellular function, including those in the intestinal epithelium, the protective layer of cells lining the gut. The TUM research team explored how impaired mitochondrial function affects the gut’s ecosystem, particularly its impact on the microbiome—the community of microorganisms residing in the intestines—which has long been associated with inflammatory bowel diseases like Crohn’s.

To investigate this connection, the researchers disrupted mitochondrial function in mice by removing a gene segment responsible for producing Hsp60, a protein essential for mitochondrial performance. This intervention resulted in noticeable tissue damage to the intestinal lining, mirroring symptoms observed in Crohn’s disease patients. Additionally, significant changes in the gut microbiome’s composition were detected, linking mitochondrial disruption to the broader impact on intestinal health.

The findings mark the first time that a direct causal relationship between mitochondrial dysfunction and both intestinal tissue damage and microbiome alterations has been established. “Our results confirm that defective mitochondria can lead to changes in the gut microbiome, which in turn exacerbates the tissue damage seen in inflammatory bowel diseases like Crohn’s,” said Dirk Haller, Chair of Nutrition and Immunology and Director of the Institute for Food and Health (ZIEL) at TUM.

This discovery opens the door to new therapeutic approaches for treating Crohn’s disease and similar conditions. Current treatments primarily focus on managing symptoms with anti-inflammatory drugs, but these new insights point toward potential interventions targeting mitochondrial function. “The hope is that by restoring mitochondrial functionality, we could mitigate intestinal damage and the subsequent chronic inflammation,” Haller explained. He added that future treatments might involve drugs that repair mitochondrial pathways or address the interactions between the mitochondria and the microbiome.

The research, published in Cell Host & Microbe, sheds light on an innovative direction for developing treatments that go beyond symptom relief and tackle the root causes of inflammation. It also underscores the importance of further exploring the connections between cellular health and microbiome dynamics.

Media Contact:

Corporate Communications Center
Anja Lapac
presse@tum.de

Contacts to this article:

Prof. Dr. Dirk Haller
Technical University of Munich
Chair of Nutrition and Immunology
Tel.: +49 8161-71 2026
dirk.haller@tum.de

SOURCE: Technical University of Munich