Evidence map›Paper›PMID 40288813›Full record

ArticleImmunoHorizons2025

PTEN inhibits scavenger receptor-mediated phagocytosis of methicillin-resistant Staphylococcus aureus.

Eden E Faneuff, Min Joo Kim, Amondrea Blackman, Kirti A Karunakaran, Jackie E Bader, Xin Zhen, Kaitlyn S Gallagher, Tanner J Durst, James A Connelly, Jeffrey C Rathmell and 3 more

Abstract read
In one paragraph

Article in ImmunoHorizons, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

13 authors.

Eden E FaneuffDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, United States.
Min Joo KimDepartment of Medicine, Division of Infectious Diseases, Vanderbilt University Medical Center, Nashville, TN, United States.
Amondrea BlackmanDepartment of Medicine, Division of Infectious Diseases, Vanderbilt University Medical Center, Nashville, TN, United States.ORCID 0000-0003-0785-938X
Kirti A KarunakaranDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, United States.
Jackie E BaderDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, United States.
Xin ZhenDivision of Genetic Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, United States.ORCID 0000-0002-4914-0413
Kaitlyn S GallagherDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, United States.ORCID 0009-0003-0802-6424
Tanner J DurstDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, United States.ORCID 0009-0007-0676-7922
James A ConnellyVanderbilt Center for Immunobiology, Vanderbilt University Medical Center, Nashville, TN, United States.ORCID 0000-0001-7223-375X
Jeffrey C RathmellDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, United States.ORCID 0000-0002-4106-3396
Ana SalinaDepartment of Medicine, Division of Infectious Diseases, Vanderbilt University Medical Center, Nashville, TN, United States.
Ruben Martinez-BarricarteDepartment of Medicine, Division of Infectious Diseases, Vanderbilt University Medical Center, Nashville, TN, United States.ORCID 0000-0001-7925-449X
Carlos Henrique SerezaniDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, United States.ORCID 0000-0002-5363-415X

Funding

Chemical Biology of Infectious Diseases (CBID) Training ProgramT32AI112541 · NIAID · VANDERBILT UNIVERSITY · PI Eric P Skaar · 2015 to 2026
$4.0M
The role of SERPINB1 in T cell function and its contribution to human diseasesR01AI168210 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Ruben Martinez Barricarte · 2023 to 2026
$2.6M
Gain-of-function complement activators as a new class of immunotherapeutic moleculesR01CA269217 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Ruben Martinez Barricarte · 2023 to 2026
$2.0M
Genetic and immunological dissection of isolated NocardiosisR21AI171466 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MARTINEZ BARRICARTE, RUBEN · 2022 to 2023
$476k
National Heart Lung and Blood Institute 5R01HL124159-09National Institute of Allergy and Infectious Diseases 5R21AI171466NCI NIH HHS 5R01CA269217NCI NIH HHS R01 CA269217NIAID NIH HHS R01 AI168210NIAID NIH HHS R21 AI171466NIAID NIH HHS T32 AI112541NIH HHS
6 · The paper itself

Abstract

Phagocytosis requires the coordination of various classes of receptors and the activation of multiple signaling programs, culminating in actin cytoskeletal rearrangement and ingestion. Given the pleiotropic nature of the events necessary for proper microbial ingestion, identifying molecules that control distinct steps of phagocytosis could reveal potential strategies to enhance microbial clearance. PTEN is a lipid/protein phosphatase traditionally recognized as a tumor suppressor. While PTEN inhibits various arms of the innate immune response, its role during Staphylococcus aureus infection remains unclear. We hypothesize that PTEN inhibits the functions of scavenger receptors (SRs) and the actin cytoskeleton during methicillin-resistant S. aureus (MRSA) infection in macrophages. RNAseq analysis of PTEN KO immortalized bone marrow-derived macrophages (iBMDMs) unveiled increased expression of genes involved in actin polymerization, pathogen recognition, and SRs, which leads to enhanced MRSA phagocytosis in both iBMDMs and primary peritoneal macrophages lacking PTEN. PTEN is physically associated with 2 SRs, MARCO and CD36, and blocking these receptors prevents the increased phagocytosis seen in PTEN KO macrophages. PTEN binds to the actin depolymerizing factor cofilin-1 during infection, inhibiting F-actin (the essential form of actin for phagocytosis) while increasing G-actin pools. Cytometry by time of flight (CyTOF) analysis of human myeloid cell populations from a PTEN-haploinsufficient patient suggests that PTEN is necessary for generating specific monocyte and dendritic subclasses. This study identifies the role of PTEN in macrophage phagocytosis of a gram-positive pathogen and in the development of monocyte subsets. This highlights the spectrum of PTEN importance in host defense mechanisms in both murine and human phagocytes.

Indexed as

MacrophagesMethicillin-Resistant Staphylococcus aureusPhagocytosisPTEN PhosphohydrolaseReceptors, ScavengerStaphylococcal InfectionsAnimalsCD36 AntigensCells, CulturedCofilin 1HumansMacrophages, PeritonealMiceMice, Inbred C57BLMice, KnockoutReceptors, ImmunologicCD36 AntigensCofilin 1Marco protein, mousePTEN PhosphohydrolasePten protein, mouseReceptors, ImmunologicReceptors, ScavengeractinphagocytosisPTENscavenger receptorsStaphylococcus aureus

Identifiers

PMID40288813
PMCPMC12034382

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

None linked

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.