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Identification of a 5-plex cytokine signature that differentiates patients with multiple systemic inflammatory diseases

Levi Hoste (UGent) , Bram Meertens (UGent) , Benson Ogunjimi, Vito Sabato, Khadija Guerti, Jeroen van der Hilst, Jeroen Bogie, Rik Joos, Karlien Claes (UGent) , Veronique Debacker (UGent) , et al.
(2025) INFLAMMATION. 48. p.2182-2197
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Abstract
Patients with non-infectious systemic inflammation may suffer from one of many diseases, including hyperinflammation (HI), autoinflammatory disorders (AID), and systemic autoimmune disease (AI). Despite their clinical overlap, the pathophysiology and patient management differ between these disorders. We aimed to investigate blood biomarkers able to discriminate between patient groups. We included 44 patients with active clinical and/or genetic systemic inflammatory disease (9 HI, 27 AID, 8 systemic AI) and 16 healthy controls. We quantified 55 serum proteins and combined multiple machine learning algorithms to identify five proteins (CCL26, CXCL10, ICAM-1, IL-27, and SAA) that maximally separated patient groups. High ICAM-1 was associated with HI. AID was characterized by an increase in SAA and decrease in CXCL10 levels. A trend for higher CXCL10 and statistically lower SAA was observed in patients with systemic AI. Principal component analysis and unsupervised hierarchical clustering confirmed separation of disease groups. Logistic regression modelling revealed a high statistical significance for HI (P = 0.001), AID, and systemic AI (P < 0.0001). Predictive accuracy was excellent for systemic AI (AUC 0.94) and AID (0.91) and good for HI (0.81). Further research is needed to validate findings in a larger prospective cohort. Results will contribute to a better understanding of the pathophysiology of systemic inflammatory disorders and can improve diagnosis and patient management.
Keywords
Cytokines, Inflammation, Biomarkers, INTERCELLULAR-ADHESION MOLECULE-1, FAMILIAL MEDITERRANEAN FEVER, INHERITED DEFECTS, EXPRESSION, AMYLOIDOSIS, RECEPTOR, AUTOINFLAMMATION, INTERLEUKIN-6, MECHANISMS, DISORDERS

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MLA
Hoste, Levi, et al. “Identification of a 5-Plex Cytokine Signature That Differentiates Patients with Multiple Systemic Inflammatory Diseases.” INFLAMMATION, vol. 48, 2025, pp. 2182–97, doi:10.1007/s10753-024-02183-3.
APA
Hoste, L., Meertens, B., Ogunjimi, B., Sabato, V., Guerti, K., van der Hilst, J., … Haerynck, F. (2025). Identification of a 5-plex cytokine signature that differentiates patients with multiple systemic inflammatory diseases. INFLAMMATION, 48, 2182–2197. https://doi.org/10.1007/s10753-024-02183-3
Chicago author-date
Hoste, Levi, Bram Meertens, Benson Ogunjimi, Vito Sabato, Khadija Guerti, Jeroen van der Hilst, Jeroen Bogie, et al. 2025. “Identification of a 5-Plex Cytokine Signature That Differentiates Patients with Multiple Systemic Inflammatory Diseases.” INFLAMMATION 48: 2182–97. https://doi.org/10.1007/s10753-024-02183-3.
Chicago author-date (all authors)
Hoste, Levi, Bram Meertens, Benson Ogunjimi, Vito Sabato, Khadija Guerti, Jeroen van der Hilst, Jeroen Bogie, Rik Joos, Karlien Claes, Veronique Debacker, Fleur Janssens, Simon Tavernier, Peggy Jacques, Steven Callens, Jo Dehoorne, and Filomeen Haerynck. 2025. “Identification of a 5-Plex Cytokine Signature That Differentiates Patients with Multiple Systemic Inflammatory Diseases.” INFLAMMATION 48: 2182–2197. doi:10.1007/s10753-024-02183-3.
Vancouver
1.
Hoste L, Meertens B, Ogunjimi B, Sabato V, Guerti K, van der Hilst J, et al. Identification of a 5-plex cytokine signature that differentiates patients with multiple systemic inflammatory diseases. INFLAMMATION. 2025;48:2182–97.
IEEE
[1]
L. Hoste et al., “Identification of a 5-plex cytokine signature that differentiates patients with multiple systemic inflammatory diseases,” INFLAMMATION, vol. 48, pp. 2182–2197, 2025.
@article{01JCWWBF16WADNP0D8D0YMFJNZ,
  abstract     = {{Patients with non-infectious systemic inflammation may suffer from one of many diseases, including hyperinflammation (HI), autoinflammatory disorders (AID), and systemic autoimmune disease (AI). Despite their clinical overlap, the pathophysiology and patient management differ between these disorders. We aimed to investigate blood biomarkers able to discriminate between patient groups. We included 44 patients with active clinical and/or genetic systemic inflammatory disease (9 HI, 27 AID, 8 systemic AI) and 16 healthy controls. We quantified 55 serum proteins and combined multiple machine learning algorithms to identify five proteins (CCL26, CXCL10, ICAM-1, IL-27, and SAA) that maximally separated patient groups. High ICAM-1 was associated with HI. AID was characterized by an increase in SAA and decrease in CXCL10 levels. A trend for higher CXCL10 and statistically lower SAA was observed in patients with systemic AI. Principal component analysis and unsupervised hierarchical clustering confirmed separation of disease groups. Logistic regression modelling revealed a high statistical significance for HI (P = 0.001), AID, and systemic AI (P < 0.0001). Predictive accuracy was excellent for systemic AI (AUC 0.94) and AID (0.91) and good for HI (0.81). Further research is needed to validate findings in a larger prospective cohort. Results will contribute to a better understanding of the pathophysiology of systemic inflammatory disorders and can improve diagnosis and patient management.}},
  author       = {{Hoste, Levi and Meertens, Bram and Ogunjimi, Benson and Sabato, Vito and Guerti, Khadija and van der Hilst, Jeroen and Bogie, Jeroen and Joos, Rik and Claes, Karlien and Debacker, Veronique and Janssens, Fleur and Tavernier, Simon and Jacques, Peggy and Callens, Steven and Dehoorne, Jo and Haerynck, Filomeen}},
  issn         = {{0360-3997}},
  journal      = {{INFLAMMATION}},
  keywords     = {{Cytokines,Inflammation,Biomarkers,INTERCELLULAR-ADHESION MOLECULE-1,FAMILIAL MEDITERRANEAN FEVER,INHERITED DEFECTS,EXPRESSION,AMYLOIDOSIS,RECEPTOR,AUTOINFLAMMATION,INTERLEUKIN-6,MECHANISMS,DISORDERS}},
  language     = {{eng}},
  pages        = {{2182--2197}},
  title        = {{Identification of a 5-plex cytokine signature that differentiates patients with multiple systemic inflammatory diseases}},
  url          = {{http://doi.org/10.1007/s10753-024-02183-3}},
  volume       = {{48}},
  year         = {{2025}},
}
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