Evidence map›Paper›PMID 37088343›Full record

ArticleThe Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation2023

Pseudomonas-dominant microbiome elicits sustained IL-1β upregulation in alveolar macrophages from lung transplant recipients.

Noel Britton, Andres Villabona-Rueda, Samantha A Whiteside, Joby Mathew, Matthew Kelley, Sean Agbor-Enoh, John F McDyer, Jason D Christie, Ronald G Collman, Andrea L Cox and 2 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Donor LungAmerican journal of respiratory cell and molecular biology · 2025
    Article
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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

12 authors at 3 institutions in 1 country.

Noel BrittonDivision of Pulmonary and Critical Care, School of Medicine, Johns Hopkins University, Baltimore, Maryland. Electronic address: rbritto2@jh.edu.
Andres Villabona-RuedaDivision of Pulmonary and Critical Care, School of Medicine, Johns Hopkins University, Baltimore, Maryland.
Samantha A WhitesideDivision of Pulmonary, Allergy, and Critical Care, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Joby MathewDivision of Pulmonary and Critical Care, School of Medicine, Johns Hopkins University, Baltimore, Maryland.
Matthew KelleyDivision of Pulmonary and Critical Care, School of Medicine, Johns Hopkins University, Baltimore, Maryland.
Sean Agbor-EnohDivision of Pulmonary and Critical Care, School of Medicine, Johns Hopkins University, Baltimore, Maryland; Laboratory of Applied Precision Omics, National Heart, Lung, and Blood Institute, Bethesda, Maryland.
John F McDyerDivision of Pulmonary, Allergy, and Critical Care, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania.
Jason D ChristieDivision of Pulmonary, Allergy, and Critical Care, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Ronald G CollmanDivision of Pulmonary, Allergy, and Critical Care, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Andrea L CoxDepartment of Medicine, Johns Hopkins University, Baltimore, Maryland.
Pali ShahDivision of Pulmonary and Critical Care, School of Medicine, Johns Hopkins University, Baltimore, Maryland.
Franco D'AlessioDivision of Pulmonary and Critical Care, School of Medicine, Johns Hopkins University, Baltimore, Maryland.
Johns Hopkins University · USUniversity of Pennsylvania · USUniversity of Pittsburgh · US

Funding

TRANSGENIC AND CHIMERIC MOUSE COREP30DK050306 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI GARY D. WU · 1997 to 2026
$32.5M
MULTIDISCIPLINARY TRAINING PROGRAM IN LUNG DISEASEST32HL007534 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Nadia N Hansel, Larissa A. Shimoda · 1985 to 2026
$28.3M
Long Term Follow up of the Lung Transplant Outcomes Group CohortU01HL145435 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI CHRISTIE, JASON D, PALMER, SCOTT M · 2019 to 2025
$10.2M
Lung Transplant Microbiome and Chronic Allograft DysfunctionR01HL113252 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI BUSHMAN, FREDERIC D, CHRISTIE, JASON D · 2013 to 2016
$2.9M
The Lung DNA Virome in Health and DiseaseR33HL137063 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI BUSHMAN, FREDERIC D, COLLMAN, RONALD G · 2019 to 2021
$2.3M
NHLBI NIH HHS R01 HL113252NHLBI NIH HHS R33 HL137063NHLBI NIH HHS T32 HL007534NHLBI NIH HHS U01 HL145435NIDDK NIH HHS P30 DK050306
6 · The paper itself

Abstract

backgroundIsolation of Pseudomonas aeruginosa (PsA) is associated with increased BAL (bronchoalveolar lavage) inflammation and lung allograft injury in lung transplant recipients (LTR). However, the effect of PsA on macrophage responses in this population is incompletely understood. We examined human alveolar macrophage (AMΦ) responses to PsA and Pseudomonas dominant microbiome in healthy LTR.

methodsWe stimulated THP-1 derived macrophages (THP-1MΦ) and human AMΦ from LTR with different bacteria and LTR BAL derived microbiome characterized as Pseudomonas-dominant. Macrophage responses were assessed by high dimensional flow cytometry, including their intracellular production of cytokines (TNF-α, IL-6, IL-8, IL-1β, IL-10, IL-1RA, and TGF-β). Pharmacological inhibitors were utilized to evaluate the role of the inflammasome in PsA-macrophage interaction.

resultsWe observed upregulation of pro-inflammatory cytokines (TNF-α, IL-6, IL-8, IL-1β) following stimulation by PsA compared to other bacteria (Staphylococcus aureus (S.Aur), Prevotella melaninogenica, Streptococcus pneumoniae) in both THP-1MΦ and LTR AMΦ, predominated by IL-1β. IL-1β production from THP-1MΦ was sustained after PsA stimulation for up to 96 hours and 48 hours in LTR AMΦ. Treatment with the inflammasome inhibitor BAY11-7082 abrogated THP-1MΦ IL-1β production after PsA exposure. BAL Pseudomonas-dominant microbiota elicited an increased IL-1β, similar to PsA, an effect abrogated by the addition of antibiotics.

conclusionPsA and PsA-dominant lung microbiota induce sustained IL-1β production in LTR AMΦ. Pharmacological targeting of the inflammasome reduces PsA-macrophage-IL-1β responses, underscoring their use in lung transplant recipients.

Indexed as

Arthritis, PsoriaticMacrophages, AlveolarCytokinesHumansInflammasomesInterleukin-6Interleukin-8LungPseudomonasTransplant RecipientsTumor Necrosis Factor-alphaUp-RegulationCytokinesInflammasomesInterleukin-6Interleukin-8Tumor Necrosis Factor-alphalung allograft injurylung transplantmacrophagemicrobiomePseudomonas aeruginosa

Identifiers

PMID37088343
PMCPMC10538944
OpenAlexW4366606864

What OpenQuestion holds

Textmetadata
LicenceTDM
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.