Cited by 334Immune Response and InflammationAntifungal resistance and susceptibilityInflammasome and immune disorders

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Dectin-1 and TLRs Permit Macrophages to Distinguish between Different Aspergillus fumigatus Cellular States

Gersuk, Geoffrey M, Underhill, David M, Zhu, Liqun, Marr, Kieren A·2006·The Journal of Immunology

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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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Self-citation

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
ORCID: Underhill, David M
Marr, Kieren A
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
DOI: 10.4049/jimmunol.176.6.3717
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
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
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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Dectin-1 and TLRs Permit Macrophages to Distinguish between Different Aspergillus fumigatus Cellular States

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