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Updated: Mar 22, 2026
Live Imaging of Antifungal Activity by Human Primary Neutrophils and Monocytes in Response to A. fumigatus
Published on: April 19, 2017
Infection-Mediated Priming of Phagocytes Protects against Lethal Secondary Aspergillus fumigatus Challenge
Amélie Savers1,2, Orhan Rasid1, Marianna Parlato3
1Institut Pasteur, Unité Cytokines & Inflammation, Paris, France.
Abstract:
Phagocytes restrict the germination of Aspergillus fumigatus conidia and prevent the establishment of invasive pulmonary aspergillosis in immunecompetent mice. Here we report that immunecompetent mice recovering from a primary A. fumigatus challenge are protected against a secondary lethal challenge. Using RAGγc knock-out mice we show that this protection is independent of T, B and NK cells. In protected mice, lung phagocytes are recruited more rapidly and are more efficient in conidial phagocytosis and killing. Protection was also associated with an enhanced expression of CXCR2 and Dectin-1 on bone marrow phagocytes. We also show that protective lung cytokine and chemokine responses are induced more rapidly and with enhanced dynamics in protected mice. Our findings support the hypothesis that following a first encounter with a non-lethal dose of A. fumigatus conidia, the innate immune system is primed and can mediate protection against a secondary lethal infection.
Insights
Innate immunity primes mice to resist lethal Aspergillus fumigatus lung infections after initial exposure. This protection relies on enhanced phagocyte function, independent of adaptive immunity.
Area of Science:
- Immunology
- Mycology
- Infectious Diseases
Background:
- Phagocytes are crucial for controlling Aspergillus fumigatus, a fungus that causes pulmonary aspergillosis.
- Immune competence is vital for preventing invasive fungal infections.
Purpose of the Study:
- To investigate if recovery from a primary Aspergillus fumigatus infection confers protection against a secondary, lethal challenge.
- To determine the immune mechanisms underlying this protection, particularly the role of innate immunity.
Main Methods:
- Utilized RAGγc knock-out mice to differentiate between innate and adaptive immune responses.
- Assessed phagocyte recruitment, phagocytosis, and killing efficiency in response to A. fumigatus.
- Measured expression of CXCR2 and Dectin-1 on phagocytes.
- Analyzed lung cytokine and chemokine profiles.
Main Results:
- Immune-competent mice recovering from an initial A. fumigatus infection were protected against a subsequent lethal challenge.
- Protection was observed in T, B, and NK cell-deficient mice, indicating an innate immune mechanism.
- Protected mice showed enhanced lung phagocyte recruitment, phagocytosis, and fungal killing.
- Upregulation of CXCR2 and Dectin-1 on bone marrow phagocytes and accelerated, enhanced lung cytokine/chemokine responses were noted.
Conclusions:
- A primary, non-lethal Aspergillus fumigatus infection primes the innate immune system.
- This primed innate immunity provides significant protection against secondary, lethal A. fumigatus challenges.
- Innate immune memory in phagocytes is a key factor in host defense against invasive pulmonary aspergillosis.
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