Lack of NLRP3-inflammasome leads to gut-liver axis derangement, gut dysbiosis and a worsened phenotype in a mouse model of NAFLD.

doi:10.1038/s41598-017-11744-6

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Article

Lack of NLRP3-inflammasome leads to gut-liver axis derangement, gut dysbiosis and a worsened phenotype in a mouse model of NAFLD.

Scientific reports - 22 Sept 2017

Pierantonelli Irene, Rychlicki Chiara, Agostinelli Laura, Giordano Debora Maria, Gaggini Melania, Fraumene Cristina, Saponaro Chiara, Manghina Valeria, Sartini Loris, Mingarelli Eleonora, Pinto Claudio, Buzzigoli Emma, Trozzi Luciano, Giordano Antonio, Marzioni Marco, Minicis Samuele De, Uzzau Sergio, Cinti Saverio, Gastaldelli Amalia, Svegliati-Baroni Gianluca

Abstract excerpt

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...

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Identifiers

PMID: 28939830
DOI: 10.1038/s41598-017-11744-6
PMCID: PMC5610266

Genes

NLRP3
TLR4
TLR9

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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