Cells (Basel, Switzerland), 2022-01, Vol.11 (2), p.182
2022
Details
- Autor(en) / Beteiligte
- Titel
- NLRP6 Inflammasome Modulates Disease Progression in a Chronic-Plus-Binge Mouse Model of Alcoholic Liver Disease
- Ist Teil von
- Cells (Basel, Switzerland), 2022-01, Vol.11 (2), p.182
- Ort / Verlag
- Switzerland: MDPI AG
- Erscheinungsjahr
- 2022
- Link zum Volltext
- Quelle
- Free E-Journal (出版社公開部分のみ）
- Beschreibungen/Notizen
- A considerable percentage of the population is affected by alcoholic liver disease (ALD). It is characterized by inflammatory signals from the liver and other organs, such as the intestine. The NLR family pyrin domain containing 6 (NLRP6) inflammasome complex is one of the most important inflammatory mediators. The aim of this study was to evaluate a novel mouse model for ALD characterized by 8-week chronic-plus-binge ethanol administration and to investigate the role of NLRP6 inflammasome for intestinal homeostasis and ALD progression using mice. We showed that chronic-plus-binge ethanol administration triggers hepatic steatosis, injury, and neutrophil infiltration. Furthermore, we discovered significant changes of intestinal microbial communities, including increased relative abundances of bacteria within the phyla and , as well as reduced . In this ALD model, inhibiting NLRP6 signaling had no effect on liver steatosis or damage, but had a minor impact on intestinal homeostasis via affecting intestinal epithelium function and gut microbiota. Surprisingly, loss resulted in significantly decreased hepatic immune cell infiltration. As a result, our novel mouse model encompasses several aspects of human ALD, such as intestinal dysbiosis. Interfering with NLRP6 inflammasome activity reduced hepatic immune cell recruitment, indicating a disease-aggravating role of NLRP6 during ALD.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 2073-4409eISSN: 2073-4409DOI: 10.3390/cells11020182Titel-ID: cdi_doaj_primary_oai_doaj_org_article_c36b46397fdd4fb39089d2520bf5296c
- Format
- –
- Schlagworte
- Acids, Adaptation, Alcohol Drinking, alcoholic liver disease, Alcoholism, ALD, Animals, Binge-Eating Disorder - metabolism, Binge-Eating Disorder - microbiology, Binge-Eating Disorder - pathology, Cecum - microbiology, Chronic Disease, Cytokines, Disease Models, Animal, Disease Progression, Dysbacteriosis, Epithelium, Ethanol, Fatty liver, Fatty Liver - complications, Fatty Liver - pathology, Gastrointestinal Microbiome, gut microbiota, Hepatitis, Homeostasis, Infiltration, inflammasome, Inflammasomes, Inflammasomes - metabolism, Inflammation, intestinal microbiota, Intestinal microflora, Intestinal Mucosa - pathology, Intestine, Laboratory animals, Leukocytes (neutrophilic), Liver - injuries, Liver - pathology, Liver cirrhosis, Liver diseases, Liver Diseases, Alcoholic - metabolism, Liver Diseases, Alcoholic - microbiology, Liver Diseases, Alcoholic - pathology, Mice, Mice, Inbred C57BL, Mice, Knockout, Microbiota, Neutrophil Infiltration, NLRP6, Pyrin protein, Receptors, Cell Surface - deficiency, Receptors, Cell Surface - metabolism, Signal Transduction, Steatosis