Researchers that study nutrition, immunology, and gastroenterology recently conducted research on an inflammatory bowel disease known as Crohn’s disease. Crohn’s disease is a chronic condition that cannot be cured. Previous research has determined that mitochondrial dysfunction and alterations in the metabolic pathways can result in impaired Paneth cells (cells lining the small intestinal tract). The lack of proper function in these cells cause the symptoms associated with Crohn’s disease. Researchers wanted to gather more specific information regarding how the mitochondria and the Paneth cells contribute to Crohn’s disease.

Tissue samples from the small intestine of patients with Crohn’s disease

Lab Mouse

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were collected and evaluated. In addition, researchers created mouse models, in which the mice exhibited mitochondrial dysfunction and inflammation similar to that of Crohn’s disease. Researchers studied the tissue samples and the mice in order to gather additional information about the disease.



I know you are eager to see the results, but there are a few logistics that I need to share. First, there is a gene that serves as the code for creating intestinal stem cells. This gene is referred to as Lgr5. Stem cells do not have a specific purpose until they go through the process of differentiation. Differentiation is when a cell is given a specific function and purpose within the body. The mitochondria is a key structure in cellular metabolism (breaking down and creating structures) and cellular metabolism controls the differentiation of a cell. When differentiation occurs, the intestinal stem cells often become Paneth cells. Paneth cells contribute to tissue regeneration and without them no new tissue could be created. When the Lgr5 gene is not functioning properly, the intestinal stem cells produced differentiate into Paneth cells that serve a different purpose from what they were supposed to. I know that was a lot of information to process, but it will help you better understand the results.

Researchers discovered that mitochondrial dysfunction results in reduced functionality of the gene Lgr5 and causes the intestinal stem cells to differentiate into Paneth cells with an abnormal function. In addition, they discovered that reduced functionality of the gene Lgr5 also correlates with intestinal inflammation in patients with Crohn’s disease and the mice with a Crohn’s like disease. This occurred because the Paneth cells developed a new function. They no longer serve as normal intestinal tissue cells. As a result, we see inflammation of the intestinal tract, the main characteristic of Crohn’s disease.

This process is rather long and complex, but it is valuable to understand the underlying causes of Crohn’s disease. Understanding how Crohn’s disease develops in the body may be the first step to creating a cure for this condition. The more we know about the disease, the better. All we can do is let the researchers do what they do best and hope that a cure is discovered in the near future.

Khaloian, S., Rath, E., Hammoudi, N., Gleisinger, E., Blutke, A., Giesbertz, P., Berger, E., Metwaly, A., Waldschmitt, N., Allez, M., & Haller, D. 2020. Mitochondrial impairment drives intestinal stem cell transition into dysfunctional Paneth cells predicting Crohn’s disease recurrence. Gut 1: 1-13.