MerTK expressing hepatic macrophages promote the resolution of inflammation in acute liver failure
Open accessAbstract
Objective: Acute liver failure (ALF) is characterised by overwhelming hepatocyte death and liver inflammation with massive infiltration of myeloid cells in necrotic areas. The mechanisms underlying resolution of acute hepatic inflammation are largely unknown. Here, we aimed to investigate the impact of Mer tyrosine kinase (MerTK) during ALF and also examine how the microenvironmental mediator, secretory leucocyte protease inhibitor (SLPI), governs this response. Design: Flow cytometry, immunohistochemistry, confocal imaging and gene expression analyses determined the phenotype, functional/transcriptomic profile and tissue topography of MerTK+ monocytes/macrophages in ALF, healthy and disease controls. The temporal evolution of macrophage MerTK expression and its impact on resolution was examined in APAP-induced acute liver injury using wild-type (WT) and Mer-deficient (Mer −/− ) mice. SLPI effects on hepatic myeloid cells were determined in vitro and in vivo using APAP-treated WT mice. Results: We demonstrate a significant expansion of resolution-like MerTK+HLA-DR high cells in circulatory and tissue compartments of patients with ALF. Compared with WT mice which show an increase of MerTK+MHCII high macrophages during the resolution phase in ALF, APAP-treated Mer −/− mice exhibit persistent liver injury and inflammation, characterised by a decreased proportion of resident Kupffer cells and increased number of neutrophils. Both in vitro and in APAP-treated mice, SLPI reprogrammes myeloid cells towards resolution responses through induction of a MerTK+HLA-DR high phenotype which promotes neutrophil apoptosis and their subsequent clearance. Conclusions: We identify a hepatoprotective, MerTK+, macrophage phenotype that evolves during the resolution phase following ALF and represents a novel immunotherapeutic target to promote resolution responses following acute liver injury.
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The existence and protective role of the MerTK+ macrophage subset have been validated in APAP-induced acute liver failure patients.
“The existence and protective role of this subset have been validated in APAP-induced acute liver failure (AALF) patients (44).”
From Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics (2026) · cites this paper as [44]
The Methods (Patients) and Results (Resolution-like MerTK+ monocytes and hepatic macrophages are expanded in ALF) establish that the study included APAP-induced ALF patients and found increased MerTK+ cells in them. The Results also report resolution-like functions in cells from ALF patients, but the direct evidence that MerTK protects against APAP-induced liver injury comes from Mer-deficient mice, not validation of a protective effect in patients. Page numbers were not provided in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredDuring the recovery phase of APAP-ALI, MerTK+ macrophages increase significantly.
“During the recovery phase of APAP-ALI, the number of Mer tyrosine kinase (MerTK)+ macrophages increases significantly.”
From Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics (2026) · cites this paper as [44]
The Results section reports an increase in the proportion of MerTK+ hepatic macrophages in APAP-treated wild-type mice at 24 and 48 hours, and the abstract places that increase in the resolution phase. Figure 3 describes statistical significance markers, but the reported mouse measure is a proportion, not the absolute number of macrophages claimed. (LLM, conf=0.84)
Experimental — accuracy not yet measuredMerTK+ macrophages efficiently clear apoptotic/necrotic cells by recognizing phosphatidylserine, and this process removes the source of damage and actively suppresses inflammation via downstream signaling.
“They efficiently clear apoptotic/necrotic cells by recognizing “eat-me” signals like phosphatidylserine. This process not only removes the source of damage but also actively suppresses inflammation via downstream signaling (44).”
From Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics (2026) · cites this paper as [44]
The Introduction (page unavailable) says MerTK recognizes phosphatidylserine on apoptotic cells and that its activation inhibits inflammatory signaling. The Results and Discussion describe enhanced clearance of apoptotic material and debris in acute liver failure. They do not establish that these macrophages recognize and clear necrotic cells through phosphatidylserine. (LLM, conf=0.84)
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- Authors
- Triantafyllou, E., Pop, O. T., Possamai, L. A., Wilhelm, A., Liaskou, E., Singanayagam, A., Bernsmeier, C., Khamri, W., Petts, G., Dargue, R., Davies, S. P., Tickle, J., Yuksel, M., Patel, V. C., Abeles, R. D., Stamataki, Z., Curbishley, S. M., Ma, Y., Wilson, I. D., Coen, M., Woollard, K. J., Quaglia, A., Wendon, J., Thursz, M. R., Adams, D. H., Weston, C. J., & Antoniades, C. G.
- Affiliations
- King's College London (GB)
- St Mary's Hospital (GB)
- University of Birmingham (GB)
- Imperial College London (GB)
- Institute of Liver Studies, King's College Hospital, King's College London, London, UK
- Corresponding author
- Antoniades, Charalambos G
- ORCID
- Triantafyllou, Evangelos
- Pop, Oltin T
- Possamai, Lucia A
- Liaskou, Evaggelia
- Singanayagam, Arjuna
- Bernsmeier, Christine
- Khamri, Wafa
- Petts, Gemma
- Dargue, Rebecca
- Davies, Scott P
- Tickle, Joseph
- Patel, Vishal C
- Abeles, Robin D
- Stamataki, Zania
- Curbishley, Stuart M
- Ma, Yun
- Wilson, Ian D
- Coen, Muireann
- Woollard, Kevin J
- Quaglia, Alberto
- Wendon, Julia
- Thursz, Mark R
- Adams, David H
- Weston, Chris J
- Venue
- Gut
- Publisher
- BMJ
- Published
- 2017-04-27
- Volume
- 67
- Issue
- 2
- Pages
- 333-347
- ISSN
- 0017-5749 (ISSN-L)
- 1468-3288
- PMC
- PMC5868289
- OpenAlex
- W2609217537
- Cited by
- 226
- References
- 43
- Citations by year
- 2026: 18 · 2025: 27 · 2024: 25 · 2023: 23 · 2022: 33 · 2021: 47 · 2020: 15 · 2019: 20 · 2018: 13 · 2017: 5
- FWCI
- 8.96
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Gut (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- St George's Online Research Archive (St George's University of London) (acceptedVersion)
- WestminsterResearch (University of Westminster) (acceptedVersion, cc-by)
- Research Portal (King's College London) (submittedVersion, cc-by)
- HighWire Press Open Archive (submittedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion, cc-by)
- Spiral (Imperial College London) (submittedVersion, other-oa)
- Funders
- National Institute for Health and Care Research (NF-SI-0512-10080, ACF-2010-21-029, CL-2015-21-002, NF-SI-0616-10012)
- Academy of Medical Sciences (SGL017\1027)
- King's College London
- University College London
- Rosetrees Trust (M115-F2, M439-F1, MR/K010514/1, M439-F1-CD2)
- National Heart and Lung Institute
- Medical Research Council (MR/M009157/1, MR/K010514/1, MC_PC_13057, MC_PC_14123)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- MERTK, acute liver failure, hepatic macrophages, inflammation resolution, secretory leukocyte protease inhibitor, Kupffer cells, neutrophil apoptosis, myeloid cells, acetaminophen hepatotoxicity, HLA-DR, neutrophil clearance, hepatoprotection
- MeSH terms
- c-Mer Tyrosine Kinase, Acetaminophen, Adult, Aged, Animals, Female, Genes, MHC Class II, HLA-DR Antigens, Humans, Kupffer Cells, Macrophages, Male, Middle Aged, Monocytes, Neutrophils, Phenotype, Gene Expression, Case-Control Studies, Liver Failure, Acute, Mice, Secretory Leukocyte Peptidase Inhibitor, Transcriptome
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