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Updated: May 21, 2026

Histological Quantification to Determine Lung Fungal Burden in Experimental Aspergillosis
Published on: March 9, 2018
Immune interaction between Aspergillus fumigatus and non-tuberculous mycobacteria
Hotaka Namie1, Takahiro Takazono1,2, Satoshi Irifune2
1Department of Infectious Diseases, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Introduction:
The global prevalence of non-tuberculous mycobacterial pulmonary disease (NTM-PD) is increasing. Individuals with NTM-PD frequently develop chronic pulmonary aspergillosis, which is associated with poor clinical outcomes. However, the biological mechanisms underlying the interaction between Aspergillus species and non-tuberculous mycobacteria (NTM) remain poorly understood. This study aimed to investigate the interaction between Aspergillus fumigatus and NTM and to identify mechanisms that may inform novel therapeutic strategies.
Methods:
A. fumigatus was incubated with NTM culture supernatants, and biofilm formation was quantified using the crystal violet assay. Phagocytic activity against A. fumigatus conidia were assessed in THP-1-derived macrophages infected with Mycobacterium avium. Conversely, phagocytosis of M. avium was evaluated in macrophages exposed to A. fumigatus culture supernatants. Finally, fungal clearance in vivo was assessed in mice pre-infected with M. avium.
Results:
NTM supernatants significantly enhanced A. fumigatus growth. M. avium infection decreased the macrophages-phagocytosis rate of A. fumigatus by approximately 40% compared to uninfected control. Additionally, M. avium infection reduced Dectin-1 gene expression in macrophages by half. Secondary metabolites produced by A. fumigatus impaired macrophage phagocytosis of M. avium. In vivo, prior M. avium infection delayed fungal clearance from the lungs.
Discussion:
NTM promote not only A. fumigatus growth but also its colonization by impairing macrophage immune function. Conversely, A. fumigatus suppresses host defense against NTM via secondary metabolites. These findings suggest that microbial cross-modulation creates a permissive niche that facilitates co-colonization and may contribute to disease progression.
Insights
Non-tuberculous mycobacteria (NTM) enhance Aspergillus growth and colonization by impairing immune cells. Aspergillus, in turn, hinders host defense against NTM, suggesting co-infections worsen disease.
Area of Science:
- Pulmonary Medicine
- Microbiology
- Immunology
Background:
- Non-tuberculous mycobacterial pulmonary disease (NTM-PD) is rising globally.
- Chronic pulmonary aspergillosis often complicates NTM-PD, leading to poor outcomes.
- Mechanisms of interaction between Aspergillus and NTM are poorly understood.
Purpose of the Study:
- Investigate the interaction between Aspergillus fumigatus and NTM.
- Identify mechanisms driving co-colonization and disease progression.
- Inform novel therapeutic strategies for NTM-PD and aspergillosis.
Main Methods:
- Assessed Aspergillus fumigatus growth in NTM culture supernatants.
- Quantified macrophage phagocytosis of Aspergillus and Mycobacterium avium.
- Evaluated fungal clearance in a mouse model of NTM infection.
Main Results:
- NTM supernatants promoted Aspergillus growth and reduced macrophage phagocytosis of Aspergillus.
- Aspergillus secondary metabolites impaired macrophage phagocytosis of Mycobacterium avium.
- Prior NTM infection delayed fungal clearance in vivo.
Conclusions:
- NTM enhance Aspergillus growth and colonization by impairing macrophage function.
- Aspergillus suppresses host defense against NTM through secondary metabolites.
- Microbial cross-modulation creates a niche for co-colonization, potentially worsening disease.
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