Evidence map›Paper›PMID 41950283›Full record

ArticlePLoS pathogens2026

Integrin ß4 is a receptor for emerging fungal pathogens from the genera Lomentospora and Scedosporium.

Povilas Kavaliauskas, Riley Risteen, Sondus Alkhazraji, Breanna Shirtliff, Thomas J Walsh, Ashraf S Ibrahim, Vincent M Bruno

Abstract read
In one paragraph

Article in PLoS pathogens, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Povilas KavaliauskasDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, United States of America.
Riley RisteenInstitute of Genome Sciences, University of Maryland School of Medicine, Baltimore, Maryland, United States of America.
Sondus AlkhazrajiDivision of Infectious Diseases, The Lundquist Institute for Biomedical Innovation, Harbor-University of California at Los Angeles (UCLA) Medical Center, Torrance, California, United States of America.
Breanna ShirtliffInstitute of Genome Sciences, University of Maryland School of Medicine, Baltimore, Maryland, United States of America.
Thomas J WalshDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, United States of America.
Ashraf S IbrahimDivision of Infectious Diseases, The Lundquist Institute for Biomedical Innovation, Harbor-University of California at Los Angeles (UCLA) Medical Center, Torrance, California, United States of America.
Vincent M BrunoDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, United States of America.ORCID 0000-0003-1683-2015

Funding

Technology CoreU19AI110820 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI RASKO, DAVID A · 2014 to 2023
$36.5M
Therapeutic targeting of growth factor receptors to treat MucormycosisR01AI141360 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI BRUNO, VINCENT MICHAEL · 2019 to 2023
$2.5M
NIAID NIH HHS R01 AI141360NIAID NIH HHS U19 AI110820
6 · The paper itself

Abstract

Lomentospora prolificans is an environmental fungus that can cause life-threatening infections when airborne conidia are inhaled. Airway epithelial cells are likely to be the first host cells to interact with L. prolificans during pulmonary infection; however, the fungal and host factors that govern this interaction are completely unknown. Herein, we combined whole fungal cell pulldowns of surface proteins from airway epithelial cells and liquid chromatography-mass spectrometry (LC-MS) to identify host proteins that could potentially serve as host receptors for the fungus. We provide evidence that integrin β4 serves as a receptor that promotes the initial binding of L. prolificans to airway epithelial cells. Integrin β4 can associate with L. prolificans conidia that have been heat-killed or pre-treated with proteinase K suggesting that the fungal ligand is not proteinaceous. Inhibition of integrin β4 function by siRNA-mediated knockdown, or blocking with an anti-integrin β4 antibody, significantly inhibited the ability of L. prolificans to adhere to human airway epithelial cells. Integrin β4 can also associate with, and promote the adherence of, two closely related species of fungal pathogens, Scedosporium apiospermum and Scedosporium boydii. Overall, our study provides novel insight into the molecular mechanisms underlying the initiation of infection by L. prolificans, and two closely related species.

Indexed as

AscomycotaIntegrin beta4MycosesScedosporiumEpithelial CellsHost-Pathogen InteractionsHumansIntegrin beta4

Identifiers

PMID41950283
PMCPMC13061235

What OpenQuestion holds

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Registered trials

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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.