Gut Microbiota-Liver Crosstalk
Nov
13
2023
Republic Ballroom
-
Sheraton Boston Hotel
2:00
- 3:30 PM EST
Speakers
Description
This session explores the intricate gut microbiota-liver crosstalk and its influence on liver disease progression, fibrosis and cirrhosis.
Abstracts
- NOVEL MECHANISMS UNDERLYING GUT LEAKINESS AND SYSTEMIC ENDOTOXEMIA IN PROMOTING LIVER FIBROSIS VIA THE GUT-LIVER AXIS AND THE MECHANISTIC PROTECTION OF MELATONIN
- ETHANOL-INDUCED REDUCTION IN THE INTESTINAL METHYLATION POTENTIAL PROMOTES TIGHT JUNCTION DISRUPTION: PROTECTION BY BETAINE TREATMENT
- MICROBIAL MONOTHERAPY WITH LEUCONOSTOC SP. LB-P8 IMPROVES INFLAMMATION AND FIBROSIS IN MOUSE MODELS OF PRIMARY SCLEROSING CHOLANGITIS.
- ALTERED SMALL AND LARGE INTESTINAL GENE EXPRESSION RELATED TO OXYGEN CONSUMPTION AND INFLAMMATION IN PATIENTS WITH CIRRHOSIS COULD CONTRIBUTE TOWARDS DYSBIOSIS AND LIVER DISEASE PROGRESSION
- GUT MICROBE-PRODUCED IMIDAZOLE PROPIONATE AGGRAVATED HEPATIC FIBROSIS BY BOOSTING HEPATOCELLULAR DEATH AND M1 MACROPHAGE POLARIZATION
- INTESTINAL EPITHELIAL CELL OSTEOPONTIN PROTECTS FROM MASH BY CHANGING THE COMPOSITION OF THE GUT MICROBIOME AND BILE ACIDS
Objectives
- Understand how altered gene expression in the intestines of patients with cirrhosis may contribute to gut dysbiosis and liver disease progression, revealing potential therapeutic targets.
- Explore the protective role of intestinal epithelial cell osteopontin in NASH by influencing the gut microbiome, providing insights into novel NASH management strategies.
- Analyze the impact of gut microbiota-derived metabolites on hepatic fibrosis and inflammation, evaluating their potential as therapeutic targets for liver diseases like primary sclerosing cholangitis and early NASH.