Evidence map›Paper›PMID 35294888›Full record

ArticleCell reports2022

L-plastin enhances NLRP3 inflammasome assembly and bleomycin-induced lung fibrosis.

Hemant Joshi, Alison Almgren-Bell, Edgar P Anaya, Elizabeth M Todd, Steven J Van Dyken, Anushree Seth, Katherine M McIntire, Srikanth Singamaneni, Fayyaz Sutterwala, Sharon C Morley

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% of its field
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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  12. Immunobiology of pulmonary fibrosis.Frontiers in immunology · 2025
    Review
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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

10 authors at 2 institutions in 1 country.

Hemant JoshiDivision of Infectious Diseases, Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA; Division of Immunobiology, Department of Immunology and Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Alison Almgren-BellDivision of Infectious Diseases, Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA; Division of Immunobiology, Department of Immunology and Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Edgar P AnayaDivision of Infectious Diseases, Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA; Division of Immunobiology, Department of Immunology and Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Elizabeth M ToddDivision of Infectious Diseases, Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA; Division of Immunobiology, Department of Immunology and Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Steven J Van DykenDivision of Immunobiology, Department of Immunology and Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Anushree SethDepartment of Mechanical Engineering and Materials Science, Institute of Materials Science and Engineering, Washington University in St. Louis, St. Louis, MO 63130, USA.
Katherine M McIntireDivision of Immunobiology, Department of Immunology and Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Srikanth SingamaneniDepartment of Mechanical Engineering and Materials Science, Institute of Materials Science and Engineering, Washington University in St. Louis, St. Louis, MO 63130, USA.
Fayyaz SutterwalaDivision of Infectious Diseases, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Sharon C MorleyDivision of Infectious Diseases, Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA; Division of Immunobiology, Department of Immunology and Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: morleys@wustl.edu.
Washington University in St. Louis · USCedars-Sinai Medical Center · US

Funding

Strength of TCR:self-pMHC interactions in the periphery instructs CD4+ T help cell responsesR01AI139540 · NIAID · WASHINGTON UNIVERSITY · PI MORLEY, SHARON CELESTE · 2019 to 2023
$2.3M
Targeting the NLRP3 inflammasome to limit pathologic sterile inflammationR01AI118719 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI SUTTERWALA, FAYYAZ S. · 2016 to 2020
$2.2M
CONTROL OF ADAPTIVE IMMUNITY BY ACTIN-REGULATORY PROTEINSR01AI104732 · NIAID · WASHINGTON UNIVERSITY · PI MORLEY, SHARON CELESTE · 2014 to 2018
$1.9M
Targeting chitin in fibrotic lung diseaseR01HL148033 · NHLBI · WASHINGTON UNIVERSITY · PI VAN DYKEN, STEVEN · 2020 to 2023
$1.7M
Multifunctional Nanoprobe for Early Appraisal of Immunotherapeutic EfficacyR21EB030171 · NIBIB · WASHINGTON UNIVERSITY · PI MORRISSEY, JEREMIAH J, SINGAMANENI, SRIKANTH · 2021 to 2022
$433k
Actin regulatory proteins regulate alveolar macrophage pro-inflammatory signalingR56AI104732 · NIAID · WASHINGTON UNIVERSITY · PI MORLEY, SHARON CELESTE · 2020 to 2020
$401k
NHLBI NIH HHS R01 HL148033NIAID NIH HHS R01 AI104732NIAID NIH HHS R01 AI118719NIAID NIH HHS R01 AI139540NIAID NIH HHS R56 AI104732NIBIB NIH HHS R21 EB030171
6 · The paper itself

Abstract

Macrophage adhesion and stretching have been shown to induce interleukin (IL)-1β production, but the mechanism of this mechanotransduction remains unclear. Here we specify the molecular link between mechanical tension on tissue-resident macrophages and activation of the NLRP3 inflammasome, which governs IL-1β production. NLRP3 activation enhances antimicrobial defense, but excessive NLRP3 activity causes inflammatory tissue damage in conditions such as pulmonary fibrosis and acute respiratory distress syndrome. We find that the actin-bundling protein L-plastin (LPL) significantly enhances NLRP3 assembly. Specifically, LPL enables apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC) oligomerization during NLRP3 assembly by stabilizing ASC interactions with the kinase Pyk2, a component of cell-surface adhesive structures called podosomes. Upon treatment with exogenous NLRP3 activators, lung-resident alveolar macrophages (AMs) lacking LPL exhibit reduced caspase-1 activity, IL-1β cleavage, and gasdermin-D processing. LPL

Indexed as

InflammasomesPulmonary FibrosisAnimalsBleomycinCaspase 1Focal Adhesion Kinase 2Interleukin-1betaMechanotransduction, CellularMembrane GlycoproteinsMiceMicrofilament ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinBleomycinCaspase 1Focal Adhesion Kinase 2InflammasomesInterleukin-1betaMembrane GlycoproteinsMicrofilament ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseplastinacute lung injurycytoskeletoninfectioninflammationlung fibrosismacrophagesmechanotransductionNLRP3 inflammasomerespiratory diseasessignal-transduction

Identifiers

PMID35294888
PMCPMC8998782
OpenAlexW4220657737

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.