Mutations in the NOD2 gene are linked to Crohn’s disease. These mutations prevent immune cells from properly switching modes, leading to inflammation. Researchers from UC San Diego utilized machine learning to analyze gene activity in immune cells from both healthy and inflamed digestive tracts.
By studying lab-grown cells, the team found that these mutations interfere with the NOD2 protein’s ability to protect against inflammatory bowel disease (IBD). They monitored immune cells called macrophages, which play crucial roles in maintaining gut health. “The gut is a battlefield, and macrophages are the peacekeepers,” explains researcher Gajanan Katkar. By mapping gene expressions, they identified how macrophages could either support healing or cause inflammation.
A significant discovery involved a protein named girdin, which works with NOD2 to keep macrophages alert without overreacting. Their collaboration is vital for gut protection. Without this partnership, macrophages struggle to manage threats effectively, leading to excessive inflammation.
When tested on mice, the absence of girdin resulted in gut inflammation and higher mortality rates due to severe immune responses. This highlights how critical these proteins are for maintaining gut balance, particularly in the context of Crohn’s disease, which results from various factors.
The research suggests potential future treatments targeting these genetic pathways to restore balance in immune response. Insights from this study may lead to new therapeutic options aimed at managing IBD more effectively.
Published in the Journal of Clinical Investigation, this research brings clarity to the molecular processes involved in gut health, paving the way for advanced treatments. For more details, you can read the full article here.
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