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Navigating the Mass Spectrometry-Based Proteomic Data Using Free Computational Tools
Published on: August 19, 2025
Proteomic analysis of serum samples of paracoccidioidomycosis patients with severe pulmonary sequel
Amanda Ribeiro Dos Santos1,2, Aline Dionizio3, Mileni da Silva Fernandes3
1Faculdade de Medicina, Universidade Federal de Mato Grosso do Sul (UFMS), Campo Grande, Brazil.
Background:
Pulmonary sequelae (PS) in patients with chronic paracoccidioidomycosis (PCM) typically include pulmonary fibrosis and emphysema. Knowledge of the molecular pathways involved in PS of PCM is required for treatment and biomarker identification.
Methodology/Principal Findings:
This non-concurrent cohort study included 29 patients with pulmonary PCM that were followed before and after treatment. From this group, 17 patients evolved to mild/ moderate PS and 12 evolved severe PS. Sera from patients were evaluated before treatment and at clinical cure, serological cure, and apparent cure. A nanoACQUITY UPLC-Xevo QT MS system and PLGS software were used to identify serum differentially expressed proteins, data are available via ProteomeXchange with identifier PXD026906. Serum differentially expressed proteins were then categorized using Cytoscape software and the Reactome pathway database. Seventy-two differentially expressed serum proteins were identified in patients with severe PS compared with patients with mild/moderate PS. Most proteins altered in severe PS were involved in wound healing, inflammatory response, and oxygen transport pathways. Before treatment and at clinical cure, signaling proteins participating in wound healing, complement cascade, cholesterol transport and retinoid metabolism pathways were downregulated in patients with severe PS, whereas signaling proteins in gluconeogenesis and gas exchange pathways were upregulated. At serological cure, the pattern of protein expression reversed. At apparent cure pathways related with tissue repair (fibrosis) became downregulated, and pathway related oxygen transport became upregulated. Additionally, we identified 15 proteins as candidate biomarkers for severe PS.
Conclusions/Significance:
Development of severe PS is related to increased expression of proteins involved in glycolytic pathway and oxygen exchange), indicative of the greater cellular activity and replication associated with early dysregulation of wound healing and aberrant tissue repair. Our findings provide new targets to study mechanisms of PS in PCM, as well as potential biomarkers.
Insights
Severe pulmonary sequelae (PS) in paracoccidioidomycosis (PCM) are linked to altered protein pathways involved in wound healing and oxygen transport. This study identifies potential biomarkers for severe PS, offering new therapeutic targets.
Area of Science:
- Pulmonary Medicine
- Proteomics
- Molecular Biology
Background:
- Chronic paracoccidioidomycosis (PCM) can lead to pulmonary sequelae (PS), including fibrosis and emphysema.
- Understanding the molecular mechanisms of PS is crucial for developing effective treatments and identifying biomarkers.
Purpose of the Study:
- To investigate the serum proteomic differences between patients with mild/moderate and severe pulmonary sequelae (PS) in chronic paracoccidioidomycosis (PCM).
- To identify molecular pathways and potential biomarkers associated with the development of severe PS in PCM.
Main Methods:
- A cohort of 29 patients with pulmonary PCM was followed before and after treatment.
- Serum samples were analyzed using UPLC-MS to identify differentially expressed proteins.
- Proteins were categorized using Cytoscape and the Reactome pathway database.
Main Results:
- Seventy-two differentially expressed proteins were found in patients with severe PS compared to mild/moderate PS.
- Key pathways altered in severe PS include wound healing, inflammatory response, and oxygen transport.
- Candidate biomarkers for severe PS were identified.
Conclusions:
- Severe PS development is associated with altered protein expression in pathways like glycolysis and oxygen exchange, suggesting dysregulated cellular activity and tissue repair.
- The findings offer new molecular targets for studying PS mechanisms and potential biomarkers for PCM.
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