ArticleJournal of neuroinflammation2024
NHH promotes Sepsis-associated Encephalopathy with the expression of AQP4 in astrocytes through the gut-brain Axis.
Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Unveiling Gut Homeostasis Disruption in Sepsis: Towards an Integrated Mechanistic and Translational Roadmap.Cell proliferation · 2026Review
- Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy.International journal of molecular sciences · 2026Review
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- Predicting 28-day and 90-day mortality in microbiologically-confirmed sepsis: a retrospective cohort study.BMC infectious diseases · 2026Article
- Endothelial-specific Ezh2 deficiency exacerbates blood-brain barrier dysfunction and neuroinflammation in sepsis-associated encephalopathy.Journal of neuroinflammation · 2026Article
- Prognostic Factors and Risk Stratification in Malignant Tumor Patients With Sepsis: A Retrospective Cohort Study.Medical science monitor : international medical journal of experimental and clinical research · 2026Article
- Glial Cells as Central Players in Neuroinflammation and Neuronal Damage Caused by Bacterial Pneumonia.Neuroimmunomodulation · 2026Review
- The brain washing system in sepsis-associated encephalopathy.Journal of neuroinflammation · 2025Review
- Cordycepin Mitigates Sepsis-Associated Encephalopathy by Promoting Microglial M2 Polarization via the IL-17a/IL-17RA/NF-κB Axis.Molecular neurobiology · 2025Article
- Acute Kidney Injury Among Patients Undergoing Orthopedic Surgery and Admitted to the ICU: A Retrospective Analysis of Nonoperative Risk Factors.Medical science monitor : international medical journal of experimental and clinical research · 2025Article
- The Crosstalk Between Sepsis-Associated Encephalopathy and Alzheimer's Disease: Identifying Potential Biomarkers and Therapeutic Targets for Cognition.Molecular neurobiology · 2025Article
- Photoacoustic imaging detects cerebrovascular pathological changes in sepsis.Photoacoustics · 2025Article
- The progress of the microbe-gut-brain axis in sepsis-associated encephalopathy.Frontiers in cellular and infection microbiology · 2025Review
- Prognostic analysis of elderly patients with pathogenic microorganisms positive for sepsis-associated encephalopathy.Frontiers in microbiology · 2024Article
- Aquaporins in sepsis- an update.Frontiers in immunology · 2024Review
- GSDMD Mediates Ang II-Induced Hypertensive Nephropathy by Regulating the GATA2/AQP4 Signaling Pathway.Journal of inflammation research · 2024Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Sepsis-associated encephalopathy (SAE) is a significant cause of mortality in patients with sepsis. Despite extensive research, its exact cause remains unclear. Our previous research indicated a relationship between non-hepatic hyperammonemia (NHH) and SAE. This study aimed to investigate the relationship between NHH and SAE and the potential mechanisms causing cognitive impairment. In the in vivo experimental results, there were no significant abnormalities in the livers of mice with moderate cecal ligation and perforation (CLP); however, ammonia levels were elevated in the hippocampal tissue and serum. The ELISA study suggest that fecal microbiota transplantation in CLP mice can reduce ammonia levels. Reduction in ammonia levels improved cognitive dysfunction and neurological impairment in CLP mice through behavioral, neuroimaging, and molecular biology studies. Further studies have shown that ammonia enters the brain to regulate the expression of aquaporins-4 (AQP4) in astrocytes, which may be the mechanism underlying brain dysfunction in CLP mice. The results of the in vitro experiments showed that ammonia up-regulated AQP4 expression in astrocytes, resulting in astrocyte damage. The results of this study suggest that ammonia up-regulates astrocyte AQP4 expression through the gut-brain axis, which may be a potential mechanism for the occurrence of SAE.
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