糖尿病,小鼠实验 z-bo 2020-09-19 511

　　The number of microorganisms in our body is 10 times that of human cells. Scientists collectively refer to all these bacteria as microbiota (microbiota). In some cases, pathogenic bacteria can cause infectious diseases. But these microorganisms can also protect us from certain diseases.

　　Researchers from Jiangnan University, the French National Institute of Health and Medical Research (INSERM), Paris Fifth University and other institutions have revealed in a recent study that the microbiota protects the human body from type 1 diabetes. The research was published in the August 4th issue of Immunity.

　　Julien Diana, member of the French National Institute of Health and Medicine, is the corresponding author of this paper. Professor Jia Sun from the School of Food Science and Technology of Jiangnan University is the first author of this paper. Professor Sun Jia’s research fields include nutritional immunity; innate defense peptides and immune health; immunomodulatory biopharmaceuticals and nutritional product development. Published a series of articles or communication SCI papers in international authoritative academic journals in the fields of immunity, allergy, and biology such as "Immunity", "Allergy", "FASEB J", and "Am J Physiol" influences.

　　In order to fight pathogens, the immune system has developed various mechanisms to detect, resist, and even eliminate microorganisms harmful to the body. This includes antimicrobial peptides and some natural proteins, which destroy these pathogens by destroying cell membranes. Not only immune cells, some cells whose functions are not related to immunity can also produce these substances.

　　The

　　research team focused on a class of multifunctional antimicrobial peptide cathelicidins with broad-spectrum antimicrobial activity. In addition to their protective functions, these antimicrobial peptides have also shown immune regulation capabilities for several autoimmune diseases. Therefore, scientists speculate that cathelicidins may be involved in the control of type 1 diabetes. Type 1 diabetes is an autoimmune disease caused by certain cells in the immune system attacking pancreatic beta cells.

　　First, they observed that pancreatic beta cells produced cathelicidins in non-diseased mice, and interestingly, cathelicidin production was impaired in diabetic mice.

　　To test this hypothesis, the researchers injected this antimicrobial peptide into diabetic mice with defective cathelicidin production. Julien Diana said: "Injection of cathelicidins inhibited the development of pancreatic inflammation and prevented these mice from developing autoimmune diseases."

　　Given that cathelicidins produce short-chain fatty acids that are controlled by intestinal bacteria, the research team investigated the possibility of short-chain fatty acids causing diabetes-related cathelicidin deficiency. Indeed, the researchers observed that diabetic mice had lower levels of short-chain fatty acids compared to healthy mice.

　　By transferring some of the intestinal bacteria from healthy mice to diabetic mice, the researchers restored normal cathelicidin levels. At the same time, the transfer of microorganisms reduces the incidence of diabetes.

　　The authors said: "This study provides further evidence that the microbiota undeniably plays a role in autoimmune diseases, especially in controlling the formation of autoimmune diabetes."

　　Preliminary data and research papers indicate that similar mechanisms may also exist in the human body, which paves the way for the development of some new treatments to combat autoimmune diabetes.