About: Inflammasome Is Activated in the Liver of Cholestatic Patients and Aggravates Hepatic Injury in Bile Duct

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About: Inflammasome Is Activated in the Liver of Cholestatic Patients and Aggravates Hepatic Injury in Bile Duct–Ligated Mouse Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Inflammasome Is Activated in the Liver of Cholestatic Patients and Aggravates Hepatic Injury in Bile Duct–Ligated Mouse
Creator	Boyer, James Cai, Shi-Ying Ge, Maoxu Hoque, Rafaz Mennone, Albert Ouyang, Xinshou
Source	PMC
abstract	BACKGROUND & AIMS: Inflammation plays an important role in the pathogenesis of cholestatic liver injury, but it is unclear whether the inflammasome is involved and is the objective of this study. METHODS: Gene expression was analyzed in the livers of patients with primary biliary cholangitis (n = 15) and primary sclerosing cholangitis (n = 15). Bile duct ligation (BDL) or sham operation was performed in wild-type (WT) and Caspase-1(–/–) (Casp1(–/–)) mice for 7 days. Mouse hepatocytes and macrophages were treated with bile acids. RESULTS: Caspase-1, NLRP1, NLRP3 and IL-1β were significantly increased in the livers of cholestatic patients when compared to healthy control subjects (n = 9). Significantly higher levels of plasma IL-1β (826 vs 345 pg/ml), ALT (674 vs 482 U/L) and ALP (900 vs 622 U/L) were seen in WT BDL mice compared to Casp1(–/–) BDL mice. Caspase-1 cleavage was found only in WT BDL livers. Assessment of liver histology indicated more fibrosis in Casp1(–/–) BDL mice than in WT BDL mice, confirmed by analyses of liver hydroxyproline content and the expression of fibrotic genes. Profiling of immune cells revealed that there were more macrophages in Casp1(–/–) BDL livers than in WT BDL livers. Further macrophage phenotype characterization indicated that Casp1(–/–) BDL livers had more M2 anti-inflammatory macrophages evidenced by more CD206 positive cells and higher expression of IL-4, CD163, Fizz1 and IL-33. When mouse hepatocytes and peritoneal macrophages were exposed to cholestatic levels of major endogenous bile acids (300μM TCA), neither IL-1β induction nor procaspase-1 cleavage were detected. CONCLUSIONS: The inflammasome exacerbates cholestatic liver injury, but bile acids do not directly activate the inflammasome.
has issue date	2019-12-27(xsd:dateTime)
bibo:doi	10.1016/j.jcmgh.2019.12.008
bibo:pmid	31887435
has license	cc-by-nc-nd
sha1sum (hex)	9a0ca44c33cfca65795894db68751ae63cc8ac7c
schema:url	https://doi.org/10.1016/j.jcmgh.2019.12.008
resource representing a document's title	Inflammasome Is Activated in the Liver of Cholestatic Patients and Aggravates Hepatic Injury in Bile Duct–Ligated Mouse
has PubMed Central identifier	PMC7160576
has PubMed identifier	31887435
schema:publication	Cell Mol Gastroenterol Hepatol
resource representing a document's body	covid:9a0ca44c33cfca65795894db68751ae63cc8ac7c#body_text
is schema:about of	named entity 'Patients' named entity 'Inflammasome' named entity 'survival rates' named entity 'inflammasome' named entity 'inflammasome' named entity 'macrophage' named entity 'macrophage' named entity 'proinflammatory' named entity 'Casp1' named entity 'liver' named entity 'hepatocytes' named entity 'endogenous' named entity 'Casp1' named entity 'liver' named entity 'serum' named entity 'immune response' named entity 'Microscopy' named entity 'bile acid' named entity 'transport proteins' named entity 'PBC' named entity 'alcoholic liver disease' named entity 'cholestatic liver injury' named entity 'biochemical' named entity 'bile acid' named entity 'caspase-1' named entity 'bile acids' named entity 'Casp1' named entity 'pathophysiological' named entity 'hepatocyte' named entity 'Cd163' named entity 'trypsin' named entity 'ATP' named entity 'inflammasome' named entity 'liver injury' named entity 'RNA' named entity 'cholestatic' named entity 'PBC' named entity 'fibrosis' named entity 'enzyme-linked immunosorbent assay' named entity 'alkaline phosphatase' named entity 'Immunohistochemistry staining' named entity 'Cyp7a1' named entity 'Kupffer cells' named entity 'hepatic injury' named entity 'homeostasis' named entity 'Cd163' named entity 'cholestasis' named entity 'fetal bovine serum' named entity 'Yale University' named entity 'GAPDH' named entity 'C57Bl' named entity 'hydroxyproline' named entity 'Liver' named entity 'hepatic injury' named entity 'inflammasome' named entity 'Plasma' named entity 'ligation' named entity 'macrophages' named entity 'pathogenesis' named entity 'pathophysiologically' named entity 'hepatocyte' named entity 'liver diseases' named entity 'inflammasome' named entity 'Immunofluorescent' named entity 'Tnfa' named entity 'cholestatic' named entity 'proinflammatory' named entity 'inflammation' named entity 'bile acids' named entity 'University of Minnesota' named entity 'bile acids' named entity 'Nlrp3' named entity 'bile acids' named entity 'Il-1b' named entity 'rotavirus' named entity 'lithocholic acid'

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