It was confirmed that enzymes that make proteins play a role in relieving inflammation in the body. It is expected that it can be applied to the diagnosis and treatment of new inflammatory diseases.
The research team led by Dr. Kim Myung-hee of the Korea Research Institute of Bioscience and Biotechnology’s Microbiome Convergence Research Center announced that they had identified the principle by which the protein synthesizing enzyme EPRS1 suppresses excessive immune responses in an inflammatory environment and maintains immunity.
Through this, it is expected that it can be used for the diagnosis of inflammatory diseases and the development of treatment technology in the future.
Inflammation is a complex immune response that occurs as a defense mechanism when a living tissue is damaged or infected. However, if this inflammation is not resolved and leads to chronic inflammation, it becomes the root of diseases that cause not only inflammatory diseases but also cardiovascular and cerebrovascular diseases and even cancer. Research on factors that induce inflammation has been actively conducted, but research on mechanisms that alleviate and eliminate inflammation is lacking.
Protein is essential to compose essential tissues of the human body and regulate metabolism, and is generally obtained through ingestion of food or through the process of making it directly in the body. It is known that 20 protein synthase enzymes are involved in the synthesis process in which cells make proteins, and 8 of them are present in the cytoplasm in a huge complex.
In a previous study, the research team found that among these eight enzyme complexes, a protein called EPRS1 has a mechanism to prevent viral infection.
In this study, the research team identified that the EPRS1 protein regulates a specific signal transduction system in the body’s inflammatory environment, such as pathogenic bacterial infection or inflammatory bowel disease, to relieve inflammation and maintain immune homeostasis.
When the EPRS1 protein is exposed to an inflammatory environment, it activates the AKT protein, which is important for signaling to suppress inflammation, and promotes the secretion of the anti-inflammatory cytokine IL-10 protein.
In an experiment using a mouse model, the research team confirmed that in the case of mice without EPRS1, when they suffer from sepsis and inflammatory bowel disease, their anti-inflammatory immune function is lowered, resulting in lower survival rates than normal mice.
Dr. Myung-Hee Kim, the research director, said, “The mechanism of EPRS1 to alleviate inflammation is to confirm that the enzyme complex, which is always present in all cells, functions not only as a protein synthesis function but also as a homeostatic mediator that regulates the body’s immune environment.” “In the future, we will contribute to the understanding of life phenomena and disease occurrence in the human body by clarifying the principles of these functions through the structural identification of enzyme complexes,” he said.
Dr. Eun-Young Lee, first author and co-corresponding author, said, “Identification of a new anti-inflammatory signaling pathway is expected to be used for the diagnosis and treatment of inflammatory diseases.”
This research was published in the online edition of Nature Communications (IF 17.694), a renowned international journal, on October 29, and was supported by the Samsung Foundation for Future Technology, the Creative Convergence Research Project of the National Science and Technology Research Council, the Biomedical Technology Development Project of the Ministry of Science and ICT, and the Life Research Institute. This was done with the support of the project.
