New approach to the therapy of chronic intestinal inflammation
Inflammatory bowel diseases are usually accompanied by a series of changes in the gut, such as an altered one Composition of the intestinal flora (gut microbiome). health-promoting gut bacteria could, according to the current study, be used in a targeted manner to counteract these changes.
researchers of University of Groningen (Netherlands) were able to decipher the causal chain that occurs in the gut chronic inflammation leads. The findings provide new approaches as to how intestinal bacteria could be used therapeutically to counteract intestinal inflammation. The research results were recently published in the journal “Gut Microbes” presents.
The role of catestatin in the gut
Catestatin is a bioactive peptide that is secreted by the intestinal mucosa. Already in one Study from 2018 the peptide has been identified as a possible target for the treatment of chronic inflammatory bowel disease identified.
Catestatin kills harmful gut bacteria
The working group around the microbiology professor Sahar El Aidy was able to prove for the first time in a mouse model that Catestatin kills bacterial strainsin turn with the development of inflammation in the intestine are connected.
The scientists genetically modified a group of mice so that they cannot produce catestatin. The mice developed signs of intestinal inflammation without the peptide.
Exchange of the intestinal flora
In further experiments, most of the intestinal flora was removed from the mice without catestatin using a laxative. The animals were then given a Stuhltransplantation the microbiome of healthy wild mice.
“We used a laxative and not antibiotics because these drugs could hinder recolonization after the fecal transplant”explains Microbiology El Aidy.
After two weeks, stool samples were taken to examine the microbial composition of the intestinal flora. Analysis of the faeces confirmed that the microbiome had shifted towards the donor – so the stool transplant was successful.
Inflammatory reactions decreased
Through an analysis of metabolites in the gut the researchers were able to document that the inflammation in the mice without catestatin by the intestinal bacteria of the healthy mice have been reduced.
With the help of the intestinal flora of the healthy animals, the mice were able to to produce short-chain fatty acids that positively influence the function of the intestine. In this way, the extent of the inflammation-related fibrosis could be contained.
Catestatin identified as an important regulator
The results suggest that the Changes in microbial composition caused by the lack of catestatin and thus an inflammatory reaction was promoted. The researchers were also able to identify a number of microbial species that are regulated by catestatin.
New approach to treating inflammatory bowel disease
Human stool transplants have had conflicting results in the past. “That could be because we didn’t know what constitutes a healthy microbial composition in humans.”concludes Professor El Aidy.
Especially the types of bacteria that are caused by the Peptide catestatin appear to be involved in inflammatory processes in the gut to be. “This is what was missing from previous attempts to restore a healthy microbial community in the gut”, sums up the head of research. (vb)
Author and source information
This text corresponds to the specifications of medical specialist literature, medical guidelines and current studies and has been checked by medical professionals.
Author:
Graduate editor (FH) Volker Blasek
Sources:
- University of Groningen: Fecal transplant throws new light on inflammatory bowel disease (published: 03.06.2022), rug.nl
- Pamela González-Dávila, Markus Schwalbe, Arpit Danewalia, et al.: Gut microbiota transplantation drives the adoptive transfer of colonic genotype-phenotype characteristics between mice lacking catestatin and their wild type counterparts; in: Gut Microbes (2022), tandfonline.com
- Elke M. Muntjewerff, Gina Dunkel, Mara J. T. Nicolasen, et al.: Catestatin as a Target for Treatment of Inflammatory Diseases; in: Frontiers in Immunology (2018), frontiersin.org
Important NOTE:
This article contains general advice only and should not be used for self-diagnosis or treatment. He can not substitute a visit at the doctor.