Abstract：
:Non-Alcoholic Fatty Liver Disease (NAFLD) represents the most common form of chronic liver injury and can progress to cirrhosis and hepatocellular carcinoma. A "multi-hit" theory, involving high fat diet and signals from the gut-liver axis, has been hypothesized. The role of the NLRP3-inflammasome, which senses dangerous signals, is controversial. Nlrp3-/- and wild-type mice were fed a Western-lifestyle diet with fructose in drinking water (HFHC) or a chow diet. Nlrp3-/--HFHC showed higher hepatic expression of PPAR γ2 (that regulates lipid uptake and storage) and triglyceride content, histological score of liver injury and greater adipose tissue inflammation. In Nlrp3-/--HFHC, dysregulation of gut immune response with impaired antimicrobial peptides expression, increased intestinal permeability and the occurrence of a dysbiotic microbiota led to bacterial translocation, associated with higher hepatic expression of TLR4 (an LPS receptor) and TLR9 (a receptor for double-stranded bacterial DNA). After antibiotic treatment, gram-negative species and bacterial translocation were reduced, and adverse effects restored both in liver and adipose tissue. In conclusion, the combination of a Western-lifestyle diet with innate immune dysfunction leads to NAFLD progression, mediated at least in part by dysbiosis and bacterial translocation, thus identifying new specific targets for NAFLD therapy.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Pierantonelli I,Rychlicki C,Agostinelli L,Giordano DM,Gaggini M,Fraumene C,Saponaro C,Manghina V,Sartini L,Mingarelli E,Pinto C,Buzzigoli E,Trozzi L,Giordano A,Marzioni M,Minicis S,Uzzau S,Cinti S,Gastaldelli A,Svegdoi
10.1038/s41598-017-11744-6subject
Has Abstractpub_date
2017-09-22 00:00:00pages
12200issue
1issn
2045-2322pii
10.1038/s41598-017-11744-6journal_volume
7pub_type
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