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Antoine Soulé

Alumni

Publications

Unbiased characterization of COVID-19 endotypes leads to prognostication of high-risk individuals using routine blood tests
William Ma
Antoine Soulé
Catherine Allard
Madeleine Durand
Karine Tremblay
Simon Rousseau
Amin Emad
Unsupervised proteomic analysis identified biologically coherent endotypes that advance understanding of acute lung injury in COVID‑19 and… (see more) support improved diagnostic and prognostic strategies.
2026-03-13
Communications Medicine (published)
doi.org
Divergent responses to SARS-CoV-2 infection in bronchial epithelium with pre-existing respiratory diseases
Justine Oliva
Manon Ruffin
Claire Calmel
Aurélien Gibeaud
Andrés Pizzorno
Clémence Gaudin
Solenne Chardonnet
Viviane de Almeida Bastos
Manuel Rosa-Calatrava
Antoine Soulé
Amin Emad
Simon Rousseau
Harriet Corvol
Olivier Terrier
Loïc Guillot
2025-02-28
iScience (published)
doi.org
Circulating IL-17F, but not IL-17A, is elevated in severe COVID-19 and leads to an ERK1/2 and p38 MAPK-dependent increase in ICAM-1 cell surface expression and neutrophil adhesion on endothelial cells
Jérôme Bédard-Matteau
Antoine Soulé
Katelyn Yixiu Liu
Lyvia Fourcade
Douglas D. Fraser
Amin Emad
Simon Rousseau
Severe COVID-19 is associated with neutrophilic inflammation and immunothrombosis. Several members of the IL-17 cytokine family have been as… (see more)sociated with neutrophilic inflammation and activation of the endothelium. Therefore, we investigated whether these cytokines were associated with COVID-19. We investigated the association between COVID-19 and circulating plasma levels of IL-17 cytokine family members in participants to the Biobanque québécoise de la COVID-19 (BQC19), a prospective observational cohort and an independent cohort from Western University (London, Ontario). We measured the in vitro impact of IL-17F on intercellular adhesion molecule 1 (ICAM-1) cell surface expression and neutrophil adhesion on endothelial cells in culture. The contribution of two Mitogen Activated Protein Kinase (MAPK) pathways was determined using small molecule inhibitors PD184352 (a MKK1/MKK2 inhibitor) and BIRB0796 (a p38 MAPK inhibitor). We found increased IL-17D and IL-17F plasma levels when comparing SARS-CoV-2-positive vs negative hospitalized participants. Moreover, increased plasma levels of IL-17D, IL-17E and IL-17F were noted when comparing severe versus mild COVID-19. IL-17F, but not IL-17A, was significantly elevated in people with COVID-19 compared to healthy controls and with more severe disease. In vitro work on endothelial cells treated with IL-17F for 24h showed an increase cell surface expression of ICAM-1 accompanied by neutrophil adhesion. The introduction of two MAPK inhibitors significantly reduced the binding of neutrophils while also reducing ICAM-1 expression at the surface level of endothelial cells, but not its intracellular expression. Overall, these results have identified an association between two cytokines of the IL-17 family (IL-17D and IL-17F) with COVID-19 and disease severity. Considering that IL-17F stimulation promotes neutrophil adhesion to the endothelium in a MAPK-dependent manner, it is attractive to speculate that this pathway may contribute to pathogenic immunothrombosis in concert with other molecular effectors.
2024-10-17
Frontiers in Immunology (published)
doi.org
Validation of ANG-1 and P-SEL as biomarkers of post-COVID-19 conditions using data from the Biobanque québécoise de la COVID-19 (BQC-19)
Eric Yamga
Antoine Soulé
Alain Piché
Amin Emad
Madeleine Durand
Simon Rousseau
2023-10-23
Clinical Proteomics (published)
doi.org
Molecular pathology of acute respiratory distress syndrome, mechanical ventilation and abnormal coagulation in severe COVID-19
Antoine Soulé
William Ma
Katelyn Yixiu Liu
Catherine Allard
Salman Qureshi
Karine Tremblay
Amin Emad
Simon Rousseau
Systemic inflammation in critically ill patients can lead to serious consequences such as acute respiratory distress syndrome (ARDS), a cond… (see more)ition characterized by the presence of lung inflammation, edema, and impaired gas exchange, associated with poor survival. Understanding molecular pathobiology is essential to improve critical care of these patients. To this end, we use multimodal profiles of SARS-CoV-2 infected hospitalized participants to the Biobanque Québécoise de la COVID-19 (BQC-19) to characterize endophenotypes associated with different degrees of disease severity. Proteomic, metabolomic, and genomic characterization supported a role for neutrophil-associated procoagulant activity in severe COVID-19 ARDS that is inversely correlated with sphinghosine-1 phosphate plasma levels. Fibroblast Growth Factor Receptor (FGFR) and SH2-containing transforming protein 4 (SHC4) signaling were identified as molecular features associated with endophenotype 6 (EP6). Mechanical ventilation in EP6 was associated with alterations in lipoprotein metabolism. These findings help define the molecular mechanisms related to specific severe outcomes, that can be used to identify early unfavorable clinical trajectories and treatable traits to improve the survival of critically ill patients.
2023-03-09
medRxiv (preprint)
doi.org
A circulating proteome-informed prognostic model of COVID-19 disease activity that relies on 1 routinely available clinical laboratories 2
William Ma
Antoine Soulé
Karine Tremblay
Simon Rousseau
Amin Emad
Abstract
2022-12-31
(published)
www.semanticscholar.org
A circulating proteome-informed prognostic model of COVID-19 disease activity that relies on routinely available clinical laboratories
William Ma
Antoine Soulé
Karine Tremblay
Simon Rousseau
Amin Emad
A minority of people infected with SARS-CoV-2 will develop severe COVID-19 disease. To help physicians predict who is more likely to require… (see more) admission to ICU, we conducted an unsupervised stratification of the circulating proteome that identified six endophenotypes (EPs) among 731 SARS-CoV-2 PCR-positive hospitalized participants in the Biobanque Québécoise de la COVID-19, with varying degrees of disease severity and times to intensive care unit (ICU) admission. One endophenotype, EP6, was associated with a greater proportion of ICU admission, ventilation support, acute respiratory distress syndrome (ARDS) and death. Clinical features of EP6 included increased levels of C-reactive protein, D-dimers, interleukin-6, ferritin, soluble fms-like tyrosine kinase-1, elevated neutrophils, and depleted lymphocytes, whereas another endophenotype (EP5) was associated with cardiovascular complications, congruent with elevated blood biomarkers of cardiovascular disease like N-terminal pro B-type natriuretic peptide (NT-proBNP), Growth Differentiation Factor-15 (GDF-15), and Troponin T. Importantly, a prognostic model solely based on clinical laboratory measurements was developed and validated on 903 patients that generalizes the EPs to new patients recruited across all pandemic waves (2020-2022) and create new opportunities for automated identification of high-risk groups in the clinic. Thus, this novel way to address pathogenesis that leverages detailed phenotypic information but relies on routinely available information in the clinic to favor translation may find applications in other diseases beyond COVID-19.
2022-11-03
medRxiv (preprint)
doi.org