Evidence map›Paper›PMID 41856108›Full record

ArticleCell host & microbe2026

Glycogen phosphorylase L confers metabolic flexibility in neutrophils to fight fungal infections in nutrient-deprived tissues.

Wonseok Choi, De-Dong Li, Colin T McLaughlin, Doureradjou Peroumal, Kiyoshi P Shiomitsu, Gillian A Moschetta, Hossein Rahimi, Shuxia Wang, Kiaan Biswas, Danielle Xie and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell host & microbe, 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

12 authors.

Wonseok ChoiDivision of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA; Department of Microbiology and Immunology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA.
De-Dong LiDivision of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA.
Colin T McLaughlinDepartment of Microbiology and Immunology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA.
Doureradjou PeroumalDivision of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA.
Kiyoshi P ShiomitsuDepartment of Microbiology and Immunology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA.
Gillian A MoschettaDepartment of Microbiology and Immunology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA.
Hossein RahimiDivision of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA; Department of Microbiology and Immunology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA.
Shuxia WangDivision of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA; Department of Medicine, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA.
Kiaan BiswasDepartment of Microbiology and Immunology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA.
Danielle XieDepartment of Microbiology and Immunology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA; Department of Medicine, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA; Center for Infectious Diseases, Stony Brook University, Stony Brook, NY 11790, USA.
Charles K VorkasDepartment of Microbiology and Immunology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA; Department of Medicine, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA; Center for Infectious Diseases, Stony Brook University, Stony Brook, NY 11790, USA.
Partha S BiswasDivision of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA; Department of Microbiology and Immunology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA. Electronic address: partha.biswas@stonybrook.edu.

Funding

RNA binding proteins in end-organ autoimmune pathologyR01AI162616 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Sarah L Gaffen · 2022 to 2026
$3.2M
Mechanisms of neutrophil dysfunction in antifungal immunityR01AI142354 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BISWAS, PARTHA SARATHI, NOLIN, THOMAS DOUGLAS · 2019 to 2023
$2.4M
Mechanisms of IL-17 Mediated Host Defense in the KidneyR01DK104680 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BISWAS, PARTHA SARATHI · 2015 to 2019
$1.5M
Identification of Mycobacterium tuberculosis-derived metabolites acting as ligands for MR1-restricted T cells.R21AI171578 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI VORKAS, CHARLES KYRIAKOS · 2023 to 2024
$468k
IL-17-epithelial cells interaction in organ damaging infectionsR21AI181831 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI BISWAS, PARTHA SARATHI · 2024 to 2025
$439k
Mechanisms of renal protection against disseminated candidiasisR21AI159058 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BISWAS, PARTHA SARATHI · 2021 to 2022
$428k
Regulation of IL-17 signaling by RNA binding proteins in kidney diseasesR21AI145242 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BISWAS, PARTHA SARATHI, GAFFEN, SARAH L · 2019 to 2020
$424k
NIAID NIH HHS R01 AI142354NIAID NIH HHS R01 AI162616NIAID NIH HHS R21 AI145242NIAID NIH HHS R21 AI159058NIAID NIH HHS R21 AI171578NIAID NIH HHS R21 AI181831NIDDK NIH HHS R01 DK104680
6 · The paper itself

Abstract

Neutrophils are crucial for defense against systemic Candida albicans infections and rely on glucose for their antifungal functions, including the production of reactive oxygen species (ROS) and neutrophil extracellular traps (NETs). In infected tissues, glucose availability is limited due to fungal consumption, posing metabolic challenges for neutrophils. We demonstrate that neutrophils overcome glucose deprivation by activating the glycogen phosphorylase liver form (PYGL) enzyme, which mobilizes intracellular glycogen stores that fuel antifungal activity. Upon C. albicans infection, fungal sensing by dectin-1 and downstream signaling through Syk and protein kinase A (PKA) kinases drive glycogenolysis in neutrophils. Neutrophil-specific deletion of PYGL in mice increases susceptibility to candidiasis, associated with defective ROS and NET generation. Treatment with a β₂-adrenergic receptor agonist, a clinically approved PYGL activator, enhances host defense in candidiasis. These findings reveal a metabolic reprogramming mechanism that supports neutrophil function in nutrient-deprived environments and identify PYGL as a potential strategy to bolster antifungal defenses.

Indexed as

Candida albicansCandidiasisGlycogen PhosphorylaseNeutrophilsAnimalsExtracellular TrapsGlucoseGlycogenMiceMice, KnockoutReactive Oxygen SpeciesSignal TransductionGlucoseGlycogenGlycogen PhosphorylaseReactive Oxygen SpeciesCandida albicansglucose deprivationglycogenimmune responseimmunometabolisminvasive candidiasiskidneyneutrophilstissue microenvironment

Identifiers

PMID41856108
PMCPMC13007716

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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.