-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
13, 2021 // -- In a recent study published in the international journal Gut, scientists from the University of Leuven and others developed a new method by studying humans and mice that can direct immune system cells to help repair tissue damage in the gut;
When functioning properly, the immune system protects the body from harmful factors, such as bacteria and viruses, but in conditions such as inflammatory bowel disease, the immune system is able to attack tissues in the intestines, creating ulcers, pain and discomfort.
about 3.9 million women and 3 million men worldwide currently suffer from inflammatory bowel disease, and the number of patients has been rising.
Because 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 symptoms of the disease, but it also interferes with the function of parts of the immune system involved in repairing damaged intestinal tissue, for example, macrophages play a key role in inflammation and tissue repair, which devours foreign invaders, cleans up debris from damaged cells, and releases special substances to guide the body's inflammation or repair process.
image source: Wikipedia/CC BY-SA 3.0 Researcher Professor Gianluca Matteoli says the idea is that the migration of macrophages to damaged tissue in inflammatory bowel disease is essential to stimulate repair of damaged areas; A series of studies were conducted to confirm this idea; when they looked at macrophages in the intestines of several patients with inflammatory bowel disease, they found a subpopulation of cells that respond to prosprosal e2 (PGE2), a messenger molecule in the immune system associated with tissue regeneration.
If a patient has an acute illness, the levels of these beneficial cells in the body are lower, and if the patient's disease is alleviated, the level of macrophages increases, suggesting that the process may also be part of the repair process.
Then the researchers turned to a mouse model of ulcerative colitis, and found that the number of prosthyroid-sensitive macrophages in the study model decreased compared to healthy mice, but if PGE2 levels increased, a small number of sensitive macrophages would react and release a special substance to stimulate tissue regeneration.
If the PGE2 subject on the macrophage is knocked out, it will cause the macrophages to stop reacting to prosthyroids, so that the level of tissue regeneration will drop, but allowing macrophages to swallow a particular lipid may restore the level of tissue regeneration, which contains a special substance that induces the release of repair stimuli.
researcher Professor Matteoli said: 'We now know that prostatin is important for inducing tissue cell proliferation, but the results of this paper show that it is also important to control the inflammatory effects of the body, so it can move the body from an acute inflammation-led phase to a repair phase.'
The prospect of developing new therapies is that lipids can activate macrophages to stimulate tissue repair, a technique that researchers have now developed and used as an experimental tool, but few such applications are available, and this is the first attempt by researchers to use them to produce beneficial therapeutic effects;
Next, researchers will explain in detail the key roles played by human macrophages in patients with inflammatory bowel disease at different stages, and finally, researcher Matteoli said, we also want to identify other factors that can shift macrophages from inflammatory cell states to non-inflammatory cell states.
then, using the liposome technology developed, we were able to target therapeutic drugs that act on macrophages and produce more precision.
() Original source: Yi Rang Na, Daun Jung, Michelle Stakenborg, et al. Prostaglandin E2 receptor PTGER4-expressing macrophages promote intestinal epithelial barrier regeneration upon inflammation, Gut (2021) doi:10.1136/gutjnl-2020-322146