Recently, published in Nature Immunology, Tiffany Horng from the Department of genetics and complex diseases of Chen Zengxi School of public health of Harvard University and Shanghai University of science and technology found that in macrophages activated by bacterial lipopolysaccharide (LPS), mitochondrial glycerol-3-phosphate dehydrogenase (gpd2) drives inflammation by regulating glucose oxidation
Gpd2 mitochondrial glycerol-3-phosphate dehydrogenase (gpd2) is an integral part of the phosphoglycerin shuttle process, which can promote glucose oxidation, promote the production of acetyl CoA, histone acetylation and the induction of genes encoding inflammatory mediators
The researchers found that although acute exposure to LPS can promote the activation of macrophages, long-term exposure to LPS can induce tolerance to LPS, and macrophages can induce immunosuppression to limit the harmful effects of persistent inflammation
The researchers also found that the transition of inflammatory response is regulated by gpd2, which coordinates the cessation of oxidative metabolism; this limits the availability of acetyl CoA for histone acetylation on genes encoding inflammatory mediators, thus helping to inhibit inflammatory response
This study shows that gpd2 and phosphoglycerin shuttle combine microbial stimulation with glucose oxidation to balance the beneficial and harmful effects of inflammation.
