Scientists understand the cause of intestinal disease in premature infants
Scientists understand the cause of intestinal disease in premature infants December 28, 2018 Source: Chinese Journal of Science In a report published in the December 12 issue of Science-Transformation Medicine, American scientists said they used necrotizing enterocolitis (NEC, a potentially fatal disease that causes premature babies to develop bowel In a mouse model of necrosis, the cause of the disease at the molecular level was found and correlated with brain damage. With this discovery, researchers will be able to work with scientists who study brain inflammation to identify potential drugs that can reverse brain damage in mice. David Hackam is Director of Child Surgery and Professor of Surgery, Pediatrics and Molecular Biology at Johns Hopkins University. He said: "There has not been a clear understanding of the cause of NEC. The only solution to serious cases is to remove the necrotic intestine of the baby by surgery. However, the surviving NEC patients still have sequelae including severe cognitive impairment. This problem has only recently made a breakthrough." Although the exact cause of neonatal NEC is unclear, scientists have known that the disease can occur in premature infants who are fed with formula and suffering from bacterial infections. Therefore, the research team developed a NEC mouse model in which newborn mice were separated from the mother and fed formula, which was placed in a hypoxic chamber twice a day as a source of pressure for 4 days. At the same time, in order to ensure that these mice carry the same pathogens as the child, the researchers will feed them with feces from severe NEC infants. According to Hackam, these mice not only have NEC, but their brains also have the same damage as humans, and brain function is also impaired in old age. Currently, they are understanding the causes of NEC-related brain damage in these mice. In this study, they first studied whether immune cells (so-called microglia) in the brains of these NEC mice were activated, and if activated, meant some inflammation. The result is that microglia are indeed activated. Other studies have shown that a protein called TLR4, combined with bacteria in the gut, can also activate microglia in the brain. The researchers then genetically engineered the mice to make the microglia contain no TLR4 and then let the mice develop NEC. The results showed that these mice did not have NEC-related brain damage, indicating that TLR4 is the cause of this injury. Next, the research team hopes to understand what substances in this intestinal disease can cause brain damage. Their previous studies showed that TLR4 protein is also present in the gut. According to Hackam, there is a high level of TLR4 in the intestine during embryonic development, but it will decline after the baby is born. In contrast, TLR4 in the gut of premature infants will remain at a high level. TLR4 in the gut of children with NEC causes the cell to release another protein, HMGB1. The team genetically engineered mice to lack HMGB1 and then contracted them with NEC. The content of microglia in the brain of these mice is less than that of mice with NEC and not genetically engineered, which means that HMGB1 produced by TLR4 in the inflamed intestine is indeed the cause of NEC-related brain damage. Hackam said: "One of the biggest strengths of our school is that we have outstanding scholars in different fields. I came here in 2014. Sujatha Kannan was one of the first colleagues I met. He was studying brain damage in rabbits. Their recent results It shows that the rabbit brain can be used for anti-cancer treatment to prevent cerebral palsy." So the two decided to cooperate to see if this method is suitable for mice with NEC. The researchers fed NEC-containing mice with antioxidant-containing nanoparticle drugs and labeled them with fluorescent molecules to examine the mouse brain and see where the luminescent molecules accumulate. In the end, they found that the area of ​​the brain that glows is the location of microglia activation. In addition, these mice have fewer activated microglia in their brains, suggesting that nanoparticle drugs protect the brain from NEC-related brain damage. Hackam said: "We really want to change our way of thinking. Don't treat NEC as a kind of intestinal disease, but treat it as a kind of intestinal-brain disease." Hackam also said: "Although this disease will immediately It is reflected in the intestines, but neonatologists should also focus on brain protection treatments, including faster surgery, bowel rest, and antibiotic use. Hackam said: "This is a devastating disease, but now we understand its foundation more clearly at the molecular level. We are eager to see if it is suitable for other models and patients, so that it is possible to ultimately better Help these babies and their parents." One Button Fast Measuring Instrument Horizontal Type One-button flash tester (horizontal) :
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