We investigated the effect of Nur77-deficiency in primary bone marrow-derived mouse macrophages and found a more pro-inflammatory phenotype. To study the role of Nur77 in acute inflammation, Nur77-deficient mice were injected with Escherichia coli bacteria establishing a peritoneal sepsis. At the onset of peritonitis Nur77 increases bacterial influx into the organs due to enhanced vascular permeability, resulting in increased tissue damage. Atherosclerosis may be considered a chronic, lipid-driven inflammation of the vessel wall. Macrophages play a crucial role in initiation and progression of this disease. We show that bone marrow-specific Nur77-deficiency aggravates atherosclerosis in dedicated mouse models. IBD represents a group of chronic inflammatory intestinal conditions. Within the last era, it has become clear that next to immunological and environmental factors, also genetic factors play an important role in the pathogenesis of IBD. In experimental colitis our data support a protective function for Nur77 in IBD.
Taken together we conclude that in acute infection Nur77 aggravates the disease, whereas this nuclear receptor has a protective function in chronic inflammation in atherosclerosis and inflammatory bowel disease.
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