Loss of NLRX1 Gene May Contribute to Bowel Disease Development, Study Shows

Loss of NLRX1 Gene May Contribute to Bowel Disease Development, Study Shows

A gene called NLRX1 plays a crucial role in inhibiting the abnormal immune system response to gastrointestinal inflammation that occurs in bowel disease, according to a study.

Loss of the gene can mean inflammatory bowel disease problems, the researchers said. Increasing the gene’s activity could be a way to fight IBD, they added.

The study, “NLRX1 Regulates Effector and Metabolic Functions of CD4T Cells,” was published in The Journal of Immunology.

Previous studies showed that loss of NLRX1 led to the production of inflammatory molecules and increased severity of bowel disease in mice.

Researchers have now discovered that when immune system T-cells lack the gene, they tend to assume an inflammatory behavior and divide into more cells, further increasing the immune system’s abnormal response.

“For decades, immunologists have applied reductionist approaches to studying the smallest details of the immune response without considering crucial systemwide interactions with nutrition and metabolism,” Josep Bassaganya-Riera, the study’s senior author, said in a news release written by Becky Freemal.

The study sheds light on novel mechanisms of immunoregulation in IBD, said Bassaganya-Riera, the CEO of BioTherapeutics, which develops nutritional and drug treatments to prevent and treat autoimmune and metabolic diseases. The research also validates computational modeling studies “that predicted the importance of NLRX1 in regulating gastrointestinal inflammation and its potential as a therapeutic target for infectious and immune-mediated diseases,” Bassaganya-Riera added.

Researchers may be able to use the findings to develop nutritional approaches to IBD and treatments that increase the NLRX1 gene’s activity in order to decrease gut inflammation.

“This seminal work, while impactful independently, sets the stage for the next lines of applied investigation on the role of NLRX1 in IBD,” said Andrew Leber, the study’s first author, who is BioTherapeutics’ scientific director. “It highlights the need to understand not only the immediately relevant pathways for novel immunoregulatory genes, but their global effect on all of the cohesive metabolic and immunological processes within a cell, a goal that we will continue to pursue.”

IBD is triggered when the immune system mistakes the body’s own microbes, food and other materials as foreign bodies and attacks the intestine, causing inflammation and damage. The faulty immune system also fails to recognize invading bacteria, making the proper functioning of the intestine even more difficult.

 

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