Reveal the molecular mechanisms and processes that turn on tissue repair in inflammatory bowel disease

  Recently, in a research report published in the international journal Gut, scientists from Leuven University and other institutions have developed a new method through research on humans and mice, which can direct immune system cells to help repair the intestinal tract Tissue damage; this may be expected to help open up effective treatments for inflammatory bowel disease, including ulcerative colitis and Crohn’s disease. When the function is normal, the immune system protects the body against harmful factors, such as bacteria and viruses, but in conditions such as inflammatory bowel disease, the immune system can attack the tissues in the intestines, resulting in ulcers, pain and the body Discomfort. Currently, approximately 3.9 million women and 3 million men worldwide suffer from inflammatory bowel disease, and the number of patients has been on the rise.

  Since the origin of inflammatory bowel disease is not clear to researchers, treatment usually focuses on how to reduce the body’s immune response to limit inflammation and the resulting disease symptoms, but this will also hinder the part of the immune system involved in repairing damaged intestinal tissues For example, macrophages play a key role in the process of inflammation and tissue repair. They swallow foreign invaders, clean up debris produced by damaged cells, and release special substances to guide the body's inflammation or repair process.

  Researcher Professor Gianluca Matteoli said that our idea is that in inflammatory bowel disease, the migration of macrophages to the damaged tissue is very necessary to stimulate the repair of the damaged part; for this reason, the researchers conducted a A series of studies confirmed this idea; when they looked at the macrophages in the intestines of many patients with inflammatory bowel disease, they found a subgroup of cells that can respond to prostaglandin E2 (PGE2), which is the immune system. Messenger molecules related to tissue regeneration.

  If the patient has an acute disease, the level of these beneficial cells in the body will be lower. If the patient's disease is relieved, the level of macrophages will increase, which indicates that this process may also be part of the repair process . Then the researchers began to study the mouse model of ulcerative colitis. They found that compared with healthy mice, the number of prostaglandin-sensitive macrophages in the tested model decreased, but if the level of PGE2 increased If so, the presence of a small number of sensitive macrophages will respond and release a special substance to stimulate tissue regeneration.

  If the PGE2 receptor on the macrophages is knocked out, the macrophages will no longer respond to prostaglandins, so the level of tissue regeneration will decrease, but the macrophages will swallow a special lipid The body may be able to restore the level of tissue regeneration. This liposome contains a special substance that can induce the release of repair stimulating factors. Researcher Professor Matteoli said that now we know that prostaglandins are very important for inducing tissue cell proliferation, but the results of this article show that it is also very important for controlling the body's inflammatory effect, so it can transfer the body from the acute stage dominated by inflammation to Repair stage.

  The prospect of developing new therapies is that liposomes can activate macrophages to stimulate tissue repair. At present, researchers have established this technology and have been widely recognized as an experimental tool, but such applications are rare, and This is also the first attempt by researchers to use it to produce beneficial therapeutic effects; later researchers still need to do more work to conduct corresponding clinical trials in patients.

  In the next step, researchers will also explain in detail the key role played by human macrophages in patients with inflammatory bowel disease at different stages; finally, the researcher Matteoli said that we also want to identify other factors that can change macrophages from inflammatory bowel disease. The cell state switches to a non-inflammatory cell state. Then using the developed liposome technology, we can target macrophages and produce more precise therapeutic drugs.