Cellular Processes That May Be Target of Future IBD Therapies Revealed in Mouse Study

Cellular Processes That May Be Target of Future IBD Therapies Revealed in Mouse Study
Cellular processes leading to the production of inflammatory cells in the gut may help explain the development of inflammatory bowel disease (IBD) and lead to new therapies, according to researchers. Their study, "IFN-γ-dependent epigenetic regulation instructs colitogenic monocyte/macrophage lineage differentiation in vivo," appeared in the journal Mucosal Immunology. Because intestines contend with more foreign substances than other parts of the body, a tight control of immune responses is key to a healthy gut. When this regulation is compromised, chronic inflammation may occur, potentially resulting in IBD. Macrophages are a type of white blood cell that that play a critical role in engulfing pathogens and dying cells. Macrophages differentiate from monocytes, another cell type, and together they contribute to IBD in the colon. But the process driving this differentiation and mediating the macrophages' ability to cause inflammation in the gut had been  unclear. Using a mouse model of IBD, scientists from Tokyo Medical and Dental University in Japan demonstrated the relevance of a cellular signaling pathway to generate colitogenic (or reactive) macrophages in the gut. The pathway contributes to the level of genes that encode inflammatory molecules, thereby increasing the production of these cells. Compared to other cells, macrophages and monocytes in the colons of IBD mice led to a greater production of proteins that promote inflammation. These cells also had greater levels of Stat1, a molecule that boosts gene levels in response to inter
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