Reduced Nicotinamide Adenine Dinucleotide Phosphate Oxidase-Independent Resistance to Aspergillus fumigatus in Alveolar Macrophages
Abstract
The fungal pathogen Aspergillus fumigatus is responsible for increasing numbers of fatal infections in immune-compromised humans. Alveolar macrophages (AM) are important in the innate defense against aspergillosis, but little is known about their molecular responses to fungal conidia in vivo. We examined transcriptional changes and superoxide release by AM from C57BL/6 and gp91phox−/− mice in response to conidia. Following introduction of conidia into the lung, microarray analysis of AM showed the transcripts most strongly up-regulated in vivo to encode chemokines and additional genes that play a critical role in neutrophil and monocyte recruitment, indicating that activation of phagocytes represents a critical early response of AM to fungal conidia. Of the 73 AM genes showing ≥2-fold changes, 8 were also increased in gp91phox−/− mice by conidia and in C57BL/6 mice by polystyrene beads, suggesting a common innate response to particulate matter. Ingenuity analysis of the microarray data from C57BL/6 mice revealed immune cell signaling and gene expression as primary mechanisms of this response. Despite the well-established importance of phagocyte NADPH oxidase in resisting aspergillosis, we found no evidence of this mechanism in AM following introduction of conidia into the mouse lung using transcriptional, luminometry, or NBT staining analysis. In support of these findings, we observed that AM from C57BL/6 and gp91phox−/− mice inhibit conidial germination equally in vitro. Our results indicate that early transcription in mouse AM exposed to conidia in vivo targets neutrophil recruitment, and that NADPH oxidase-independent mechanisms in AM contribute to inhibition of conidial germination.
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Much of the discrepancy in the literature on killing of Aspergillus conidia by AMs is related to differences in study endpoints, methodology of killing assessment, moiety of infection, infection time points, NADPH oxidase knockout mouse strains, and method of immunosuppression.
“much of the discrepancy in the literature is related to differences in study endpoints (e.g., inhibition of growth versus killing), methodology of killing assessment (e.g., CFU plating versus conidial germination), moiety of infection, infection time points, NADPH oxidase knockout mouse strains, and method of immunosuppression used (203, 240–245).”
From Aspergillus fumigatus and Aspergillosis in 2019 (2019) · cites this paper as [243]
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- Authors
- Cornish, E. J., Hurtgen, B. J., McInnerney, K., Burritt, N. L., Taylor, R. M., Jarvis, J. N., Wang, S. Y., & Burritt, J. B.
- Affiliations
- Montana State University (US)
- OU Health (US)
- Corresponding author
- McInnerney, Kate
- ORCID
- Jarvis, James N
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-05
- Volume
- 180
- Issue
- 10
- Pages
- 6854-6867
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1569957341
- Cited by
- 48
- References
- 82
- Citations by year
- 2026: 1 · 2023: 2 · 2022: 2 · 2021: 1 · 2019: 4 · 2018: 3 · 2017: 3 · 2016: 3 · 2015: 2 · 2014: 4 · 2013: 4 · 2012: 3
- FWCI
- 3.43
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r03ai057931-02)
- National Institute of Allergy and Infectious Diseases (1 R03 AI 057931-01)
- National Center for Research Resources (P20RR020185)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Keywords
- Aspergillus fumigatus, aspergillosis, alveolar macrophages, NADPH oxidase, gp91phox, conidial germination, superoxide release, chemokines, neutrophil recruitment, innate immunity, transcriptional response, particulate matter, immune cell signaling
- MeSH terms
- Animals, Aspergillosis, Aspergillus fumigatus, Bronchoalveolar Lavage Fluid, Enzyme-Linked Immunosorbent Assay, Lung Diseases, Fungal, Macrophage Activation, Male, Mice, Inbred C57BL, Mice, Mutant Strains, RNA, Messenger, Spores, Fungal, Superoxides, Transcription, Genetic, Gene Expression, Macrophages, Alveolar, NADPH Oxidases, Reverse Transcriptase Polymerase Chain Reaction, Oligonucleotide Array Sequence Analysis, Mice
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