Evidence map›Paper›PMID 33156984›Full record

ArticleChronic obstructive pulmonary diseases (Miami, Fla.)2021

Black Carbon Content in Airway Macrophages is Associated with Reduced CD80 Expression and Increased Exacerbations in Former Smokers With COPD.

Vickram Tejwani, Eric Moughames, Karthik Suresh, Shih-En Tang, Laura G Mair, Karina Romero, Nirupama Putcha, Neil E Alexis, Han Woo, Franco R D'Alessio and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Chronic obstructive pulmonary diseases (Miami, Fla.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

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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

11 authors at 4 institutions in 2 countries.

Vickram TejwaniJohns Hopkins University, Division of Pulmonary and Critical Care Medicine, Baltimore, Maryland, United States.
Eric MoughamesJohns Hopkins Bayview Medical Center, Baltimore, Maryland, United States.
Karthik SureshJohns Hopkins University, Division of Pulmonary and Critical Care Medicine, Baltimore, Maryland, United States.
Shih-En TangDivision of Pulmonary and Critical Care Medicine, Tri-Service General Hospital, Taipei, Taiwan.
Laura G MairJohns Hopkins Bayview Medical Center, Baltimore, Maryland, United States.
Karina RomeroJohns Hopkins Bayview Medical Center, Baltimore, Maryland, United States.
Nirupama PutchaJohns Hopkins University, Division of Pulmonary and Critical Care Medicine, Baltimore, Maryland, United States.
Neil E AlexisDepartment of Pediatrics, University of North Carolina, Chapel Hill, North Carolina, United States.
Han WooJohns Hopkins University, Division of Pulmonary and Critical Care Medicine, Baltimore, Maryland, United States.
Franco R D'AlessioJohns Hopkins University, Division of Pulmonary and Critical Care Medicine, Baltimore, Maryland, United States.
Nadia N HanselJohns Hopkins University, Division of Pulmonary and Critical Care Medicine, Baltimore, Maryland, United States.
Johns Hopkins University · USTri-Service General Hospital · TWUniversity of North Carolina at Chapel Hill · USJohns Hopkins Medicine · US

Funding

The Environmental Assessments Core (FSC)P50MD010431 · NIMHD · JOHNS HOPKINS UNIVERSITY · PI MATSUI, ELIZABETH C. · 2015 to 2019
$3.5M
Clinical trial of air cleaners to improve indoor air quality and COPD healthR01ES022607 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI HANSEL, NADIA N · 2013 to 2017
$3.4M
Metabolic regulation of Ca2+ entry and endothelial-mesenchymal transition in pulmonary arterial hypertensionR01HL151530 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SURESH, KARTHIK · 2021 to 2025
$2.0M
ROS-induced endothelial dysfunction in pulmonary arterial hypertensionK08HL132055 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SURESH, KARTHIK · 2017 to 2021
$828k
Macrophage phenotype and COPD severityF32HL149258 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TEJWANI, VICKRAM · 2019 to 2020
$145k
Johns Hopkins Eudowood FoundationNHLBI NIH HHS F32 HL149258NHLBI NIH HHS F32HL149258-01NHLBI NIH HHS K08 HL132055NHLBI NIH HHS R01 HL151530NIEHS NIH HHS R01 ES022607NIMHD NIH HHS P50 MD010431the Department of Defense DoDW81XWH-16-1-0510the National Institute of Environmental Health Sciences of the National Institutes of Health R01ES022607the National Institute on Minority Health and Health Disparities of the National Institutes of Health P50MD010431the U.S.Environmental Protection Agency 83615001
6 · The paper itself

Abstract

backgroundChronic obstructive pulmonary disease (COPD) is characterized by recurrent exacerbations. Macrophages play a critical role in immune response and tissue repair in COPD. Airway macrophages (AM) are exposed to environmental exposures which are retained in the cytoplasmic material. Both biomass and particulate matter have been linked to higher AM black carbon. It is unknown if AM black carbon is associated with COPD morbidity and macrophage phenotype.

methodsFormer smokers with COPD were enrolled and sputum induction was performed to obtain airway macrophages. Macrophages underwent black carbon quantification and flow cytometry phenotyping. Health information was obtained the same day as sputum induction and prospective exacerbations were assessed by monthly telephone calls.

resultsWe studied 30 former smokers with COPD who had a mean age of 67 years and mean forced expiratory volume in 1 second (FEV

conclusionAM black carbon association with respiratory morbidity is largely unexplored and this is the first study to identify association with prospective exacerbations. Macrophages expressed reduced CD80, a surface marker providing costimulatory signals required for development of antigen-specific immune responses. Our findings suggest that reduced CD80 expression is the pathophysiologic mechanism for the association of AM black carbon content and increased exacerbations. Therefore, beyond solely serving as a marker for increased exposures, AM black carbon content may be a predictor of future exacerbations given a macrophage less equipped to respond to an acute infectious exposure.

Indexed as

black carbonCD80COPDMacrophage

Identifiers

PMID33156984
PMCPMC8047619
OpenAlexW3095063884

What OpenQuestion holds

Textmetadata
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.