AI Article Synopsis
- Interactions between the host and its gut microbiota, like Helicobacter hepaticus, are beneficial and promote health through various molecular mechanisms.
- In the absence of proper IL-10 signaling, H. hepaticus can lead to inflammation in the intestines by activating IL-23, but it also induces early IL-10 in immune cells for regulation.
- The study identifies a polysaccharide produced by H. hepaticus that activates an anti-inflammatory response through TLR2, highlighting potential pathways for new treatments for inflammatory bowel disease.
Article Abstract
Interactions between the host and its microbiota are of mutual benefit and promote health. Complex molecular pathways underlie this dialog, but the identity of microbe-derived molecules that mediate the mutualistic state remains elusive. Helicobacter hepaticus is a member of the mouse intestinal microbiota that is tolerated by the host. In the absence of an intact IL-10 signaling, H. hepaticus induces an IL-23-driven inflammatory response in the intestine. Here we investigate the interactions between H. hepaticus and host immune cells that may promote mutualism, and the microbe-derived molecule(s) involved. Our results show that H. hepaticus triggers early IL-10 induction in intestinal macrophages and produces a large soluble polysaccharide that activates a specific MSK/CREB-dependent anti-inflammatory and repair gene signature via the receptor TLR2. These data identify a host-bacterial interaction that promotes mutualistic mechanisms at the intestinal interface. Further understanding of this pathway may provide novel prevention and treatment strategies for inflammatory bowel disease.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5734933 | PMC |
| http://dx.doi.org/10.1016/j.chom.2017.11.002 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Probiotic Mixture Attenuates Colorectal Tumorigenesis in Murine AOM/DSS Model by Suppressing STAT3, Inducing Apoptotic p53 and Modulating Gut Microbiota.
Probiotics Antimicrob Proteins
December 2024
School of Biological Sciences, University of Hong Kong, Pokfulam, Hong Kong, 999077, China.
Colorectal cancer (CRC) is one of the most common cancers worldwide. The standard CRC chemo drug, 5-Fluorouracil (5-FU), has a poor response rate and chemoresistance, prompting the need for a more effective and affordable treatment. In this study, we aimed to evaluate whether Prohep, a novel probiotic mixture, would alleviate azoxymethane/dextran sodium sulfate (AOM/DSS)-induced colorectal tumorigenesis and enhance 5-FU efficacy and its mechanism.
View Article and Find Full Text PDFStudy on the molecular mechanisms of rifaximin in the treatment of non‑alcoholic steatohepatitis based on the ‑DCA‑Fxr‑Hnf1α signalling pathway.
Mol Med Rep
February 2025
Department of Gastroenterology, Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Article Synopsis
- * Mice fed a methionine-choline deficient diet to induce NASH were treated with rifaximin, which significantly reduced liver fat, inflammation, and fibrosis.
- * Rifaximin was found to change gut microbiota and inhibit the intestinal DCA-Fxr-Hnf1α signaling pathway, suggesting its potential for treating NASH clinically.
Hesperidin and Fecal Microbiota Transplantation Modulate the Composition of the Gut Microbiota and Reduce Obesity in High Fat Diet Mice.
Diabetes Metab Syndr Obes
October 2024
Department of Anorectal Surgery, the Tenth Affiliated Hospital of Southern Medical University (Dongguan People's Hospital), Dongguan, People's Republic of China.
Article Synopsis
- Obesity is linked to issues like gut microbiota imbalance, inflammation, and intestinal barrier dysfunction, and flavonoids like hesperidin may provide safe anti-obesity solutions.
- In experiments with high-fat diet (HFD)-fed mice, hesperidin treatment reduced body weight, fat accumulation, inflammation markers, and improved gut health, showing a dose-dependent effect.
- Both hesperidin and fecal microbiota transplantation (FMT) successfully reduced body weight and addressed HFD-related disorders by altering gut microbiota composition.
Helicobacter pylori and Campylobacter jejuni bacterial holocytochrome c synthase structure-function analysis reveals conservation of heme binding.
Commun Biol
August 2024
Department of Biological Sciences, University of Delaware, Newark, DE, 19716, USA.
Heme trafficking is essential for cellular function, yet mechanisms of transport and/or heme interaction are not well defined. The System I and System II bacterial cytochrome c biogenesis pathways are developing into model systems for heme trafficking due to their functions in heme transport, heme stereospecific positioning, and mediation of heme attachment to apocytochrome c. Here we focus on the System II pathway, CcsBA, that is proposed to be a bi-functional heme transporter and holocytochrome c synthase.
View Article and Find Full Text PDFExperimental colonization with H. hepaticus, S. aureus and R. pneumotropicus does not influence the metabolic response to high-fat diet or incretin-analogues in wildtype SOPF mice.
Mol Metab
September 2024
Core Facility Laboratory Animal Services, Helmholtz Munich, Germany.
Objectives: We here assessed whether typical pathogens of laboratory mice affect the development of diet-induced obesity and glucose intolerance, and whether colonization affects the efficacy of the GLP-1R agonist liraglutide and of the GLP-1/GIP co-agonist MAR709 to treat obesity and diabetes.
Methods: Male C57BL/6J mice were experimentally infected with Helicobacter hepaticus, Rodentibacter pneumotropicus and Staphylococcus aureus and compared to a group of uninfected specific and opportunistic pathogen free (SOPF) mice. The development of diet-induced obesity and glucose intolerance was monitored over a period of 26 weeks.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!