ArticlePLoS pathogens2016
FleA Expression in Aspergillus fumigatus Is Recognized by Fucosylated Structures on Mucins and Macrophages to Prevent Lung Infection.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 52 citations in OpenAlex.
- COVID-19-Associated Fungal Co-Infections: Pathogenesis, Diagnostics, Biomarkers, and Therapeutic Strategies.Journal of clinical medicine · 2026Review
- Requirement for Fucosyltransferase 2 in Allergic Airway Hyperreactivity and Mucus Obstruction.American journal of respiratory cell and molecular biology · 2025Article
- Could the Lung Be a Gateway for Amphotericin B to Attack the Army of Fungi?Pharmaceutics · 2022Review
- Novel Treatment Approach for Aspergilloses by Targeting Germination.Journal of fungi (Basel, Switzerland) · 2022Review
- Fungal-mediated lung allergic airway disease: The critical role of macrophages and dendritic cells.PLoS pathogens · 2022Review
- Respiratory Epithelial Cells: More Than Just a Physical Barrier to Fungal Infections.Journal of fungi (Basel, Switzerland) · 2022Review
- Review
- Genetically increased circulating FUT3 level leads to reduced risk of idiopathic pulmonary fibrosis: a Mendelian randomisation study.The European respiratory journal · 2022Article
- Pathogenesis of Respiratory Viral and Fungal Coinfections.Clinical microbiology reviews · 2022Review
- Highly sialylated mucin-type glycopeptide from porcine intestinal mucosa after heparin extraction: O-glycan profiling and immunological activity evaluation.Glycoconjugate journal · 2021Article
- Genomic and Phenotypic Analysis of COVID-19-Associated Pulmonary Aspergillosis Isolates of Aspergillus fumigatus.Microbiology spectrum · 2021Article
- Biochemical and structural studies of target lectin SapL1 from the emerging opportunistic microfungus Scedosporium apiospermum.Scientific reports · 2021Article
- Sensing the threat posed by Aspergillus infection.Current opinion in microbiology · 2020Review
- Genomic and phenotypic analysis of COVID-19-associated pulmonary aspergillosis isolates ofbioRxiv : the preprint server for biology · 2020Article
- Bronchial Epithelial Cells on the Front Line to Fight Lung Infection-CausingFrontiers in immunology · 2020Review
- Aspergillus fumigatus and Aspergillosis in 2019.Clinical microbiology reviews · 2019Review
- Antivirulence and avirulence genes in human pathogenic fungi.Virulence · 2019Review
- Menacing Mold: Recent Advances in Aspergillus Pathogenesis and Host Defense.Journal of molecular biology · 2019Review
- Conidial surface proteins at the interface of fungal infections.PLoS pathogens · 2019Review
- Mucociliary Defense: Emerging Cellular, Molecular, and Animal Models.Annals of the American Thoracic Society · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
The immune mechanisms that recognize inhaled Aspergillus fumigatus conidia to promote their elimination from the lungs are incompletely understood. FleA is a lectin expressed by Aspergillus fumigatus that has twelve binding sites for fucosylated structures that are abundant in the glycan coats of multiple plant and animal proteins. The role of FleA is unknown: it could bind fucose in decomposed plant matter to allow Aspergillus fumigatus to thrive in soil, or it may be a virulence factor that binds fucose in lung glycoproteins to cause Aspergillus fumigatus pneumonia. Our studies show that FleA protein and Aspergillus fumigatus conidia bind avidly to purified lung mucin glycoproteins in a fucose-dependent manner. In addition, FleA binds strongly to macrophage cell surface proteins, and macrophages bind and phagocytose fleA-deficient (∆fleA) conidia much less efficiently than wild type (WT) conidia. Furthermore, a potent fucopyranoside glycomimetic inhibitor of FleA inhibits binding and phagocytosis of WT conidia by macrophages, confirming the specific role of fucose binding in macrophage recognition of WT conidia. Finally, mice infected with ΔfleA conidia had more severe pneumonia and invasive aspergillosis than mice infected with WT conidia. These findings demonstrate that FleA is not a virulence factor for Aspergillus fumigatus. Instead, host recognition of FleA is a critical step in mechanisms of mucin binding, mucociliary clearance, and macrophage killing that prevent Aspergillus fumigatus pneumonia.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.