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Updated: May 22, 2026

Efficient Method for Imaging Murine Lungs that Preserves Spatial Dynamics of Fungal Spores in the Airways
Published on: December 13, 2024
Characterisation of innate fungal recognition in the lung
Inês Faro-Trindade1, Janet A Willment, Ann M Kerrigan
1Division of Immunology, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory, South Africa.
Abstract:
The innate recognition of fungi by leukocytes is mediated by pattern recognition receptors (PRR), such as Dectin-1, and is thought to occur at the cell surface triggering intracellular signalling cascades which lead to the induction of protective host responses. In the lung, this recognition is aided by surfactant which also serves to maintain the balance between inflammation and pulmonary function, although the underlying mechanisms are unknown. Here we have explored pulmonary innate recognition of a variety of fungal particles, including zymosan, Candida albicans and Aspergillus fumigatus, and demonstrate that opsonisation with surfactant components can limit inflammation by reducing host-cell fungal interactions. However, we found that this opsonisation does not contribute directly to innate fungal recognition and that this process is mediated through non-opsonic PRRs, including Dectin-1. Moreover, we found that pulmonary inflammatory responses to resting Aspergillus conidia were initiated by these PRRs in acidified phagolysosomes, following the uptake of fungal particles by leukocytes. Our data therefore provides crucial new insights into the mechanisms by which surfactant can maintain pulmonary function in the face of microbial challenge, and defines the phagolysosome as a novel intracellular compartment involved in the innate sensing of extracellular pathogens in the lung.
Insights
Pulmonary surfactant limits fungal inflammation by reducing leukocyte interactions. Innate fungal recognition occurs via Dectin-1 and other PRRs within acidified phagolysosomes, not through surfactant opsonization.
Area of Science:
- Immunology
- Pulmonary Medicine
- Microbiology
Background:
- Leukocyte recognition of fungi involves pattern recognition receptors (PRRs) like Dectin-1, initiating host defense.
- Pulmonary surfactant influences inflammation and lung function, but its role in fungal recognition is unclear.
Purpose of the Study:
- To investigate pulmonary innate recognition of fungi.
- To determine the role of surfactant in fungal recognition and inflammation.
- To identify the cellular compartments involved in sensing fungal pathogens.
Main Methods:
- Exposure of leukocytes to fungal particles (zymosan, Candida albicans, Aspergillus fumigatus).
- Assessment of fungal recognition and inflammatory responses.
- Analysis of surfactant opsonization effects on host-cell fungal interactions.
- Investigation of PRR involvement and intracellular signaling pathways.
Main Results:
- Surfactant opsonization limits inflammation by reducing host-cell fungal interactions but does not mediate direct innate recognition.
- Innate fungal recognition is mediated by non-opsonic PRRs, including Dectin-1.
- Pulmonary inflammatory responses to Aspergillus conidia are initiated by PRRs within acidified phagolysosomes after fungal uptake.
Conclusions:
- Surfactant maintains pulmonary function during fungal challenge by modulating inflammatory responses.
- Acidified phagolysosomes are identified as a novel intracellular site for innate sensing of extracellular fungal pathogens by leukocytes.
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