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Updated: Oct 25, 2025
Author Spotlight: Unveiling the Polyfunctionality and Heterogeneity in Immune Responses
Published on: March 8, 2024
The cytokines HGF and CXCL13 predict the severity and the mortality in COVID-19 patients
Matthieu Perreau1, Madeleine Suffiotti1, Pedro Marques-Vidal2
1Service of Immunology and Allergy, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Insights
Researchers identified key cytokine biomarkers, hepatocyte growth factor (HGF) and C-X-C motif chemokine ligand 13 (CXCL13), that predict severe COVID-19 progression and ICU admission. These markers also indicate a higher likelihood of death in patients.
Area of Science:
- Immunology
- Virology
- Critical Care Medicine
Background:
- Severe COVID-19 is characterized by dysregulated immune responses.
- Predictive biomarkers for intensive care unit (ICU) admission and mortality in COVID-19 patients are crucial for clinical management.
- Understanding the immunological signatures of severe disease can guide therapeutic strategies.
Purpose of the Study:
- To identify immunological markers that predict ICU admission in patients with severe coronavirus disease 2019 (COVID-19).
- To validate these predictive markers in independent patient cohorts.
- To explore the association of identified markers with patient mortality.
Main Methods:
- Investigated over 170 immunological markers in a discovery cohort (n=98) from Lausanne University Hospital (LUH-1).
- Analyzed cytokine and cellular markers for association with ICU admission across three cohorts (LUH-1, French COVID-19 Study (FCS), LUH-2).
- Assessed the predictive value of combined markers (HGF and CXCL13) for ICU admission and mortality.
Main Results:
- Thirteen out of 49 cytokines significantly predicted ICU admission (P < 0.05 to P < 0.001).
- Cellular immunological markers showed limited power in discriminating between ICU and non-ICU patients.
- The combination of hepatocyte growth factor (HGF) and C-X-C motif chemokine ligand 13 (CXCL13) demonstrated high predictive values for ICU admission and identified an 8.8-fold increased likelihood of death.
Conclusions:
- HGF and CXCL13 serve as robust biomarkers for predicting severe COVID-19 outcomes, including ICU admission and mortality.
- The interplay between HGF (anti-inflammatory, tissue repair) and CXCL13 (pro-inflammatory, fibrosis) reflects a critical host immune response in severe COVID-19.
- These findings highlight the potential of cytokine profiling for risk stratification and management of COVID-19 patients.
Abstract:
The objective of the present study was to identify biological signatures of severe coronavirus disease 2019 (COVID-19) predictive of admission in the intensive care unit (ICU). Over 170 immunological markers were investigated in a 'discovery' cohort (n = 98 patients) of the Lausanne University Hospital (LUH-1). Here we report that 13 out of 49 cytokines were significantly associated with ICU admission in the three cohorts (P < 0.05 to P < 0.001), while cellular immunological markers lacked power in discriminating between ICU and non-ICU patients. The cytokine results were confirmed in two 'validation' cohorts, i.e. the French COVID-19 Study (FCS; n = 62) and a second LUH-2 cohort (n = 47). The combination of hepatocyte growth factor (HGF) and C-X-C motif chemokine ligand 13 (CXCL13) was the best predictor of ICU admission (positive and negative predictive values ranging from 81.8% to 93.1% and 85.2% to 94.4% in the 3 cohorts) and occurrence of death during patient follow-up (8.8 fold higher likelihood of death when both cytokines were increased). Of note, HGF is a pleiotropic cytokine with anti-inflammatory properties playing a fundamental role in lung tissue repair, and CXCL13, a pro-inflammatory chemokine associated with pulmonary fibrosis and regulating the maturation of B cell response. Up-regulation of HGF reflects the most powerful counter-regulatory mechanism of the host immune response to antagonize the pro-inflammatory cytokines including CXCL13 and to prevent lung fibrosis in COVID-19 patients.
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