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Updated: May 24, 2026
Histological Quantification to Determine Lung Fungal Burden in Experimental Aspergillosis
Published on: March 9, 2018
G-CSF enhances neutrophil function with potential involvement of INHBA during Aspergillus fumigatus infection
Wenxin Zhang1, Haitao Wang2, Majid S Jabir3
1Department of Pathology, The First Hospital of Jilin University, Changchun 130021, China; Key Laboratory of Pathobiology, Medical Basic Research Innovation Center of Airway Disease in North China, Ministry of Education, Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun 130021, China.
Introduction:
Aspergillus fumigatus causes life-threatening infections in immunocompromised individuals. Neutrophils are essential for antifungal defence, but their function is often impaired in these patients. Granulocyte colony-stimulating factor (G-CSF) supports neutrophil survival and activation, yet systemic use can induce unwanted inflammation. The molecular mechanisms by which G-CSF enhances neutrophil function remain incompletely defined.
Objectives:
To investigate whether ex vivo G-CSF-activated neutrophil transfer improves outcomes in invasive A. fumigatus infection and to explore the potential involvement of INHBA in regulating neutrophil dysfunction.
Methods:
Immunosuppressed mice were intranasally infected with A. fumigatus and subsequently received intravenous administration of G-CSF-activated neutrophils. Fungal burden, pulmonary inflammation, and cytokine expression were assessed. Transcriptomic and single-cell RNA sequencing analyses identified pathways regulated by G-CSF and INHBA. In vitro assays examined the impact of recombinant INHBA on neutrophil functions.
Results:
Transfer of G-CSF-activated neutrophils significantly improved survival, reduced fungal load, and decreased lung inflammation. G-CSF downregulated INHBA, while patient neutrophils displayed elevated INHBA expression. Functional studies showed INHBA suppressed neutrophil chemotaxis, phagocytosis, and NET formation.
Conclusion:
G-CSF enhances neutrophil antifungal activity and is associated with modulation INHBA, suggesting a potential regulatory axis in neutrophil dysfunction during A. fumigatus infection. Ex vivo G-CSF-activated neutrophil transfer may represent a promising immunotherapeutic strategy for invasive aspergillosis.
Insights
Granulocyte colony-stimulating factor (G-CSF) enhances neutrophil function against Aspergillus fumigatus. G-CSF-activated neutrophil transfer improves outcomes in invasive aspergillosis by modulating INHBA, offering a potential immunotherapy.
Area of Science:
- Immunology
- Infectious Diseases
- Cell Biology
Background:
- Aspergillus fumigatus causes severe infections in immunocompromised patients.
- Neutrophil dysfunction impairs antifungal defense in these individuals.
- Granulocyte colony-stimulating factor (G-CSF) supports neutrophils but can cause inflammation; its mechanisms are unclear.
Purpose of the Study:
- To evaluate ex vivo G-CSF-activated neutrophil transfer for invasive A. fumigatus infection.
- To investigate the role of INHBA in G-CSF-mediated neutrophil regulation and dysfunction.
Main Methods:
- Immunosuppressed mice with A. fumigatus infection received G-CSF-activated neutrophils.
- Fungal burden, inflammation, and cytokine levels were measured.
- Transcriptomic, single-cell RNA sequencing, and in vitro assays explored G-CSF and INHBA pathways.
Main Results:
- G-CSF-activated neutrophil transfer improved survival and reduced fungal load and lung inflammation.
- G-CSF downregulated INHBA expression, while patient neutrophils showed elevated INHBA.
- INHBA suppressed neutrophil chemotaxis, phagocytosis, and NET formation.
Conclusions:
- G-CSF enhances neutrophil antifungal activity via INHBA modulation, indicating a regulatory axis in neutrophil dysfunction.
- Ex vivo G-CSF-activated neutrophil transfer shows promise as an immunotherapy for invasive aspergillosis.
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