Research & Publications | Ji Laboratory | Loyola University Chicago

Research Focus

The Ji Laboratory studies the molecular basis underlying acute respiratory distress syndrome (ARDS), sepsis, and lung sarcoidosis. Our research aims to study new phenotypes, endotypes, druggable targets, biomarkers, and predictive models that can benefit personalized medicine (precision medicine).

Our key research areas include:

Clustering Endotypes for Subphenotypes: Applying cutting-edge techniques including metaproteomics, host trans-omics, and machine learning to identify endotypes and biomarkers.
Modeling Pulmonary Critical Diseases: Develop predictive models to precisely predict the outcomes and treatment responses.
Fibrinolytic System in Injured Lungs: Studying the critical role of fibrinolysis and lung epithelial proteins in COVID-19 and edema fluid resolution.
Validation of Crucial Function of Diseased Genes: Examining how SFTPC and Wnt pathways affect alveolar epithelial cell fate in fibrotic lungs.
Epithelial Sodium Channels in Lung Injury: Investigating the role of ENaC in the pathogenesis of lung edema using humanized SCNN1D knockin mouse models.

Research Areas in Detail

Endotype Clustering

We utilize multi-omics approaches and advanced machine learning techniques to identify novel endotypes and biomarkers for pulmonary diseases. This precision medicine approach allows for better patient stratification and personalized treatment.

Predictive Modeling

Development of sophisticated predictive models using clinical and multi-omics data to forecast patient outcomes and treatment responses. Our models incorporate machine learning algorithms to improve accuracy and clinical utility.

Fibrinolytic System

Investigation of the fibrinolytic system's role in lung injury and repair, with particular focus on COVID-19 and acute respiratory distress syndrome. Our work has revealed critical roles for fibrinolysis in alveolar epithelial cell function.

Gene Function Validation

Examining the functional roles of key genes in pulmonary disease pathogenesis, with emphasis on SFTPC and Wnt signaling pathways. We employ advanced techniques including CRISPR-Cas9 genome editing, 3D organoids, and humanized mouse models.

ENaC in Lung Injury

Studying epithelial sodium channels (ENaC) in lung edema resolution and injury. Our laboratory has pioneered research on humanized SCNN1D knockin mouse models to understand how ENaC function influences pulmonary edema pathogenesis.

Scholarly Publications

The Ji Laboratory is committed to advancing scientific knowledge through rigorous research and scholarly publication. Our work focuses on understanding the molecular mechanisms of pulmonary conditions, with particular emphasis on lung injury, repair, and host-pathogen interactions.

For a complete and up-to-date list of our publications, please visit the following resources:

NCBI My Bibliography Google Scholar

These profiles are automatically updated with our latest publications. For PDF requests or additional information, please contact us.

Google Scholar

ResearchGate

3,500+

Citations

35+

H-Index

20+

Research Collaborations

100+

Publications

Featured Publications

A selection of our most impactful recent work

Fibrinolytic niche is required for alveolar type 2 cell-mediated alveologenesis

Signal Transduction and Targeted Therapy (2021)

Study investigating the critical role of fibrinolysis in AT2 cell-mediated re-alveolarization.

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Associations of D-dimer on admission and clinical features of COVID-19 patients

Frontiers in Immunology (2021)

Meta-analysis examining the relationship between D-dimer levels and COVID-19 severity.

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TRIM72 promotes alveolar epithelial cell membrane repair and ameliorates lung fibrosis

Respiratory Research (2020)

Research exploring membrane repair mechanisms in alveolar epithelial cells and implications for IPF.

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Ion transport mechanisms for smoke inhalation–injured airway epithelial barrier

Cell Biology and Toxicology (2020)

Investigation of how thermal stress and smoke aldehydes affect airway epithelial barrier function.

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Fibrinolytic or anti-plasmin (nafamostat) therapy for COVID-19

Pulmonary Pharmacology & Therapeutics (2021)

Discussion of timing considerations for fibrinolytic and anti-plasmin therapies in COVID-19 treatment.

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Elevated plasmin(ogen) as a common risk factor for COVID-19 susceptibility

American Physiological Society (2020)

Study showing how elevated plasmin(ogen) in patients with comorbidities promotes SARS‑CoV‑2 spike protein cleavage and hyperfibrinolysis.

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Recent Publications

Our latest scientific contributions

2024

Cao P, Ji HL, Sun J

Pulmonary fibrosis and endocrine factors

Frontiers in Endocrinology, 15, 1519318

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Pulmonary fibrosis (PF) is a complex and highly heterogeneous disease characterized by the accumulation of stiffened extracellular matrix in lung tissue, the replacement of normal lung tissue with fibrotic tissue, and the progressive loss of lung function. PF is induced by genetic, environmental, and inflammatory factors and is associated with metabolic disorders. This research topic aims to define the endogenous factors associated with pulmonary fibrosis to facilitate the discovery of novel and effective therapeutic strategies with fewer side effects.

2024

Xi NM, Ji HL, Wang L

Understanding Sarcoidosis Using Large Language Models and Social Media Data

Journal of Healthcare Informatics Research, 1-26

View Paper

Sarcoidosis is a rare inflammatory disease characterized by the formation of granulomas in various organs. In this study, we employed a Large Language Model (LLM) to analyze sarcoidosis-related discussions on Reddit. Our findings underscore the efficacy of LLMs in accurately identifying sarcoidosis-related content. We discovered a wide array of symptoms reported by patients, with fatigue, swollen lymph nodes, and shortness of breath as the most prevalent. Prednisone was the most prescribed medication, while infliximab showed the highest effectiveness in improving prognoses.

2024

Jain KG, Liu Y, Zhao R, Muire PJ, Xi NM, Ji HL

Surfactant Protein-C Regulates Alveolar Type 2 Epithelial Cell Lineages via the CD74 Receptor

Journal of Respiratory Biology and Translational Medicine, 1(4), 10017

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Deficiency of surfactant protein-C (SPC) increases susceptibility to lung infections and injury, and suppressed expression of SPC has been associated with the severity of acute respiratory distress syndrome (ARDS). This study aimed to investigate the mechanisms by which SPC regulates AT2 lineages. We utilized three-dimensional (3D) organoids to compare AT2 lineage characteristics between wild type (WT) and Sftpc−/− mice by analyzing AT2 proliferation, alveolar type 1 cells (AT1) differentiation and CD74 expression.

2024

Jain KG, Liu Y, Zhao R, Muire PJ, Zhang J, Zang QS, Ji HL

Humanized L184Q Mutated Surfactant Protein C Gene Alters Alveolar Type 2 Epithelial Cell Fate

International Journal of Molecular Sciences, 25(16), 8723

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Alveolar type 2 epithelial (AT2) cells synthesize surfactant protein C (SPC) and repair an injured alveolar epithelium. A mutated surfactant protein C gene (SftpcL184Q, Gene ID: 6440) in newborns has been associated with respiratory distress syndrome and pulmonary fibrosis. We utilized three-dimensional (3D) feeder-free AT2 organoids in vitro to simulate the alveolar epithelium and compared AT2 lineage characteristics between WT (C57BL/6) and SftpcL184Q mutant mice. The study revealed significant impacts of this mutation on AT2 cellular behavior.

2024

Xi NM, Ji HL, Vasilopoulos A, Zhao R

PROTEOMIC IDENTIFICATION OF REGENERATIVE NICHES AND DRUGGABLE TARGETS FOR ARDS LUNGS

SHOCK, 62(1), 100-100

View Paper

Abstract not available

2024

Vasilopoulos A, Xi NM, Zhao R, Ji HL

CLINICAL VARIABLE-BASED PREDICTION OF ACUTE RESPIRATORY DISTRESS SYNDROME ENDOTYPES

SHOCK, 62(1), 18-19

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Abstract not available

2021

Ali G, Zhang M, Zhao R, Jain KG, Chang J, Komatsu S, Zhou B, Liang J, Matthay MA, Ji HL

Fibrinolytic niche is required for alveolar type 2 cell-mediated alveologenesis via a uPA-A6-CD44+-ENaC signal cascade

Signal Transduction and Targeted Therapy, 6(1), 97

View Paper

Alveolar type 2 epithelial (AT2) cells are stem cells of the distal lung and are critical for alveolar regeneration. This study investigated how the fibrinolytic system supports AT2 cell-mediated alveologenesis. Using 3D organoid models and genetically modified mice, the researchers identified a crucial signaling pathway involving urokinase-type plasminogen activator (uPA), annexin A6, CD44, and epithelial sodium channels (ENaC) that facilitates AT2 cell-mediated repair and regeneration in injured lungs.

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Research Collaborations

Our research benefits from collaborations with leading scientists and clinicians from across the world

Clinical Partners

Department of Surgery, Loyola University Chicago
Burn and Shock Trauma Research Institute
Loyola University Medical Center
Department of Medicine, Division of Pulmonary and Critical Care

Academic Collaborators

Northwestern University
University of Chicago
University of Texas
National Institutes of Health
Harvard Medical School

Industry Partners

Pharmaceutical Research Labs
Biotechnology Companies
Medical Device Manufacturers
Computational Biology Firms

Funding Sources

Our research is generously supported by grants from various funding agencies:

National Institutes of Health

R01, R21 Grants

Loyola University Chicago

Internal Research Awards

We are grateful for the continued support that makes our research possible.