The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Dectin-1 and TLRs Permit Macrophages to Distinguish between Different Aspergillus fumigatus Cellular States
Abstract
Aspergillus fumigatus is a common cause of invasive and allergic pulmonary disease. Resting conidia of the filamentous fungus are constantly inhaled, but cause infection only after initiating hyphal growth. In this study, we have explored whether macrophages can distinguish between resting spores and the maturing, potentially invasive form of the fungus. Although macrophages bind and ingest A. fumigatus resting conidia efficiently, there is little inflammatory response; NF-κβ is not activated, inflammatory cytokines are not induced, and reactive oxygen species are not produced. However, maturing A. fumigatus conidia and germ tubes stimulate NF-κβ, secretion of proinflammatory cytokines and production of reactive oxygen by human monocyte-derived macrophages and murine macrophages from multiple anatomical sites. These responses are in part mediated by dectin-1, which binds cell wall β-glucan that is not present on the surface of dormant conidia, but is present after cellular swelling and loss of the hydrophobic proteinaceous cell wall. Dectin-1 binding to germ tubes augments, but is not required for, TLR2-mediated inflammatory cytokine secretion. Dectin-1 recognition of germ tubes also stimulates TNF-α production in the absence of both TLR2 and MyD88 signaling. These data demonstrate one mechanism by which the pulmonary inflammatory response is tailored toward metabolically active cells, thereby avoiding unnecessary tissue damage with frequent inhalation of ubiquitous spores.
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“The discovery of selective activation of Dectin-1/Syk signaling during germination of Aspergillus conidia due to stage-specific surface exposure of β-glucan (194, 246, 247) and the ability of PRR to regulate phagosome maturation (248) provided the conceptual framework of pathogen-associated molecular patterns (PAMPs) masking as a mechanism employed by fungi to escape macrophage killing.”
From Aspergillus fumigatus and Aspergillosis in 2019 (2019) · cites this paper as [247]
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Aspergillus fumigatus and Aspergillosis in 2019
Latgé, J.-P., & Chamilos, G. (2019) · Clinical Microbiology Reviews · doi:10.1128/cmr.00140-18 · Cited by 1,400
Dectin-1 is required for β-glucan recognition and control of fungal infection
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Infections Caused by Scedosporium spp
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Dyken, S. J. V., & Locksley, R. M. (2013) · Annual Review of Immunology · doi:10.1146/annurev-immunol-032712-095906 · Cited by 743
Metadata
- Authors
- Gersuk, G. M., Underhill, D. M., Zhu, L., & Marr, K. A.
- Affiliations
- University of Washington (US)
- Cedars-Sinai Medical Center (US)
- Corresponding author
- Zhu, Liqun
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2006-03
- Volume
- 176
- Issue
- 6
- Pages
- 3717-3724
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1562117121
- Cited by
- 334
- References
- 31
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 4 · 2023: 10 · 2022: 6 · 2021: 10 · 2020: 9 · 2019: 15 · 2018: 14 · 2017: 22 · 2016: 16 · 2015: 18 · 2014: 23 · 2013: 15 · 2012: 16
- FWCI
- 12.14
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM62995, R01GM062995)
- National Institute of Allergy and Infectious Diseases (R01 AI51468, R01AI051468)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- Aspergillus fumigatus, Dectin-1, TLR2, macrophages, germ tube, conidia, β-glucan, NF-κB, TNF-α, reactive oxygen species, inflammatory cytokines, lung inflammation, fungal pathogenesis, MyD88, innate immunity
- MeSH terms
- Dectin-1, Animals, Aspergillus fumigatus, Cell Differentiation, Cells, Cultured, Humans, Inflammation, Macrophages, Membrane Proteins, Nerve Tissue Proteins, Protein Binding, Tumor Necrosis Factor-alpha, Lectins, C-Type, Toll-Like Receptor 2, Toll-Like Receptor 4, Mice
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