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Peer-reviewedCC BY 4.0PLOS One

Dysregulation of the serum and IgG N-glycome in decompensated cirrhosis and its association with Model for End-Stage Liver Disease-Sodium (MELD-Na)

  • Andreea Cislaru1
  • Emre Yagmur2
  • Catherine Bannon3
  • Sinead Cremen4
  • Tom K. Gallagher5
  • Danilo Sarti6
  • Mark W. Robinson7
  • Róisín O’Flaherty
7 affiliations
  1. 1Department of Chemistry, Maynooth University, Maynooth, Co. Kildare, Ireland
  2. 2Kathleen Lonsdale Institute for Human Health Research, Maynooth University, Maynooth, Co. Kildare, Ireland
  3. 3Department of Biology, Maynooth University, Maynooth, Co. Kildare, Ireland
  4. 4School of Medicine, University College Dublin, Belfield, Dublin, Ireland
  5. 5Department of Hepatopancreaticobiliary and Transplant Surgery, St. Vincent’s University Hospital, Elm Park, Dublin, Ireland
  6. 6Royal College of Surgeons in Ireland, University of Medicine and Health Sciences, Saint Stephen’s Green, Dublin, Ireland
  7. 7CÚRAM, Science Foundation Ireland Research Centre for Medical Devices, Biomedical Sciences, University of Galway, Co. Galway, Ireland
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Abstract

Background and Aims: N-glycans modulate glycoprotein structure and function and are altered during chronic inflammation. We sought to define the extent of serum and IgG N-glycan disruption in patients with decompensated liver cirrhosis from alcohol-related liver disease (ALD), primary sclerosing cholangitis (PSC), and ALD-related hepatocellular carcinoma (HCC). Finally, we aimed to examine whether serum and IgG glycosylation is associated with changes in Model for End-stage Liver Disease-Sodium (MELD-Na) scores, a clinical marker used to prioritise liver transplantation. Methods: Serum samples were obtained from patients with ALD (n = 17), PSC (n = 7), ALD-related HCC (n = 4), and healthy controls (n = 10). N-glycans were released, fluorescently labelled, and profiled by hydrophilic interaction ultra performance liquid chromatography (HILIC-UPLC). Chromatograms were integrated into 46 and 23 glycan peaks for serum and IgG respectively. These peaks and their associated glycosylation traits were statistically compared with healthy controls using age- and sex-adjusted linear regression models. Results: In serum, decompensated cirrhosis shows statistically significant shifts toward less complex, agalactosylated and asialylated biantennary glycans, accompanied by significant losses of highly branched, galactosylated and sialylated structures. IgG mirrored this pattern, which is characteristic of a pro-inflammatory signature, with increased agalactosylation and bisected glycan levels, along with reduced levels of digalactosylated and sialylated species. N-glycan profiles showed significant associations with MELD-Na scores, indicating that inflammatory processes in decompensated liver cirrhosis continue to reshape serum glycoproteins. Conclusion: Decompensated liver cirrhosis shows profound remodelling of serum and IgG N-glycans. These data establish a reference framework for terminal glycomic disruption in liver disease and highlight the potential value of incorporating glycosylation analysis into broader assessments of liver disease progression.

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Cite

BibTeXRIS
BibTeX
@article{cislaru2026dysregulation,
  title = {{Dysregulation of the serum and IgG N-glycome in decompensated cirrhosis and its association with Model for End-Stage Liver Disease-Sodium (MELD-Na)}},
  author = {Andreea Cislaru and Emre Yagmur and Catherine Bannon and Sinead Cremen and Tom K. Gallagher and Danilo Sarti and Mark W. Robinson and Róisín O’Flaherty},
  journal = {PLOS One},
  year = {2026},
  month = sep,
  doi = {10.1371/journal.pone.0357709},
  url = {https://doi.org/10.1371/journal.pone.0357709},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Dysregulation of the serum and IgG N-glycome in decompensated cirrhosis and its association with Model for End-Stage Liver Disease-Sodium (MELD-Na)
AU  - Andreea Cislaru
AU  - Emre Yagmur
AU  - Catherine Bannon
AU  - Sinead Cremen
AU  - Tom K. Gallagher
AU  - Danilo Sarti
AU  - Mark W. Robinson
AU  - Róisín O’Flaherty
PY  - 2026
DA  - 2026/09/15
JO  - PLOS One
DO  - 10.1371/journal.pone.0357709
UR  - https://doi.org/10.1371/journal.pone.0357709
AB  - Background and Aims: N-glycans modulate glycoprotein structure and function and are altered during chronic inflammation. We sought to define the extent of serum and IgG N-glycan disruption in patients with decompensated liver cirrhosis from alcohol-related liver disease (ALD), primary sclerosing cholangitis (PSC), and ALD-related hepatocellular carcinoma (HCC). Finally, we aimed to examine whether serum and IgG glycosylation is associated with changes in Model for End-stage Liver Disease-Sodium (MELD-Na) scores, a clinical marker used to prioritise liver transplantation. Methods: Serum samples were obtained from patients with ALD (n = 17), PSC (n = 7), ALD-related HCC (n = 4), and healthy controls (n = 10). N-glycans were released, fluorescently labelled, and profiled by hydrophilic interaction ultra performance liquid chromatography (HILIC-UPLC). Chromatograms were integrated into 46 and 23 glycan peaks for serum and IgG respectively. These peaks and their associated glycosylation traits were statistically compared with healthy controls using age- and sex-adjusted linear regression models. Results: In serum, decompensated cirrhosis shows statistically significant shifts toward less complex, agalactosylated and asialylated biantennary glycans, accompanied by significant losses of highly branched, galactosylated and sialylated structures. IgG mirrored this pattern, which is characteristic of a pro-inflammatory signature, with increased agalactosylation and bisected glycan levels, along with reduced levels of digalactosylated and sialylated species. N-glycan profiles showed significant associations with MELD-Na scores, indicating that inflammatory processes in decompensated liver cirrhosis continue to reshape serum glycoproteins. Conclusion: Decompensated liver cirrhosis shows profound remodelling of serum and IgG N-glycans. These data establish a reference framework for terminal glycomic disruption in liver disease and highlight the potential value of incorporating glycosylation analysis into broader assessments of liver disease progression.
SN  - 1932-6203
ER  -