ArticleNature communications2018
Macrophage-derived IL-1β/NF-κB signaling mediates parenteral nutrition-associated cholestasis.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 109 citations in OpenAlex.
- Farnesoid X receptor activates STAT3 to promote fatty acid oxidation and suppress inflammatory macrophage responses in cholestasis.The Journal of biological chemistry · 2026Article
- Single-nucleus RNA sequencing uncovers cell type-specific alterations in OSA-related liver injury.Scientific reports · 2026Article
- Dietary Lauric Acid Suppresses Inflammation, Cholestasis, Hepatocyte Injury, and Senescence in 3,5-Diethoxycarbonyl-1,4-Dihydrocollidine-induced Inflammatory Cholangiopathy.Cellular and molecular gastroenterology and hepatology · 2026Article
- High-Throughput Metabolomics in Transfusion Medicine.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Identification of prognostic-related tumor microenvironment genes in lung adenocarcinoma and establishment of a prognostic prediction model.Translational lung cancer research · 2025Article
- Intestinal failure-associated liver disease model: a reduced phytosterol intravenous lipid emulsion prevents liver injury.Pediatric research · 2025Article
- Multicomponent parenteral lipid emulsions do not prevent liver injury in neonatal pigs with obstructive cholestasis.JCI insight · 2025Article
- Curcumin: A Natural Warrior Against Inflammatory Liver Diseases.Nutrients · 2025Review
- Asparagine transporter supports macrophage inflammation via histone phosphorylation.Science advances · 2025Article
- Pathogenesis and Management of Intestinal Failure-Associated Liver Disease.Seminars in liver disease · 2025Review
- Metabolic insights into hypoxia adaptation in adolescent athletes at different altitudes: a cross-sectional study.Frontiers in molecular biosciences · 2025Article
- MRPL35 Attenuates Neonatal Parenteral Nutrition-Associated Cholestasis by Modulating the ROS/JNK/NF-κB Pathway.Journal of inflammation research · 2025Article
- Parenteral nutrition results in peripheral ileal to hepatic circadian discordance in mice.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Hepatic Gα13 ablation shifts region-specific colonic inflammatory status by modulating the bile acid synthetic pathway in mice.Scientific reports · 2024Article
- Linking NLRP3 inflammasome and pulmonary fibrosis: mechanistic insights and promising therapeutic avenues.Inflammopharmacology · 2024Review
- How traditional Chinese medicine can prevent recurrence of common bile duct stones after endoscopic retrograde cholangiopancreatography?Frontiers in pharmacology · 2024Review
- Bile Acids Promote Hepatic Biotransformation and Excretion of Aflatoxin B1 in Broiler Chickens.Toxins · 2023Article
- Altered hepatic and intestinal homeostasis in a neonatal murine model of short-term total parenteral nutrition and antibiotics.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Metabolic signatures of cardiorenal dysfunction in plasma from sickle cell patients as a function of therapeutic transfusion and hydroxyurea treatment.Haematologica · 2023Article
- High glucose enhances the activation of NLRP3 inflammasome by ambient fine particulate matter in alveolar macrophages.Particle and fibre toxicology · 2023Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 3 countries.
Funding
Abstract
In infants intolerant of enteral feeding because of intestinal disease, parenteral nutrition may be associated with cholestasis, which can progress to end-stage liver disease. Here we show the function of hepatic macrophages and phytosterols in parenteral nutrition-associated cholestasis (PNAC) pathogenesis using a mouse model that recapitulates the human pathophysiology and combines intestinal injury with parenteral nutrition. We combine genetic, molecular, and pharmacological approaches to identify an essential function of hepatic macrophages and IL-1β in PNAC. Pharmacological antagonism of IL-1 signaling or genetic deficiency in CCR2, caspase-1 and caspase-11, or IL-1 receptor (which binds both IL-1α and IL-1β) prevents PNAC in mice. IL-1β increases hepatocyte NF-κB signaling, which interferes with farnesoid X receptor and liver X receptor bonding to respective promoters of canalicular bile and sterol transporter genes (Abcc2, Abcb11, and Abcg5/8), resulting in transcriptional suppression and subsequent cholestasis. Thus, hepatic macrophages, IL-1β, or NF-κB may be targets for restoring bile and sterol transport to treat PNAC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.