Inflammatory bowel disease (IBD) is a category of refractory inflammatory disease, of which ulcerative colitis (UC) and Crohn’s disease (CD) are the main types.
Currently, researchers have found that IBD is a complex auto-inflammatory disease determined by genetic and environmental factors, and is the major cause of gastrointestinal cancer.
Because of its complex and refractory character, researchers have focused on determining the detailed pathogenesis of IBD and finding an effective therapy for it.
In a new study, scientists found a new mechanism involved in the development of IBD and suggested treatment targets.
The research was conducted by a team at the Chinese Academy of Sciences and elsewhere.
Among the identified IBD-susceptibility genes, the extracellular matrix protein-1 (ECM1) gene was found to be strongly related to ulcerative colitis in 2008.
Since 2011, several studies have reported the disease-related functions of ECM1 in cells. However, no available evidence suggested that ECM1 plays a direct role in IBD.
In this study, the researchers analyzed tissue samples from patients with ulcerative colitis and an IBD mice model.
They found that ECM1 was highly expressed in macrophages, particularly under inflammatory conditions, and ECM1 expression was strongly induced during IBD progression.
A macrophage is a large white blood cell that is an important part of the immune system.
Further study showed that ECM1 protein could regulate M1 macrophage polarization.
These results reveal a role for the IBD-susceptibility gene ECM1 in colitis, indicating that the decrease of the ECM1 function is a possible strategy for IBD therapy.
The study is published in PNAS.
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