Evidence map›Paper›PMID 29940963›Full record

ArticleRespiratory research2018

Comparison of pro- and anti-inflammatory responses in paired human primary airway epithelial cells and alveolar macrophages.

Reem Al Mubarak, Nicole Roberts, Robert J Mason, Scott Alper, Hong Wei Chu

Open access · goldAbstract readComparative Study
In one paragraph

Article in Respiratory research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 30% 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

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

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Recognition of Mycobacterium tuberculosis by macrophage Toll-like receptor and its role in autophagy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Review
  8. Article
  9. Article
  10. ReplicativebioRxiv : the preprint server for biology · 2023
    Article
  11. Article
  12. Article
  13. Review
  14. Identifying the Risk of Acute Exacerbation in Idiopathic Pulmonary Fibrosis: A Step Forward.American journal of respiratory and critical care medicine · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

5 authors at 2 institutions in 1 country.

Reem Al MubarakDepartment of Medicine, National Jewish Health, 1400 Jackson Street, Room A639, Denver, CO, 80206, USA.
Nicole RobertsDepartment of Medicine, National Jewish Health, 1400 Jackson Street, Room A639, Denver, CO, 80206, USA.
Robert J MasonDepartment of Medicine, National Jewish Health, 1400 Jackson Street, Room A639, Denver, CO, 80206, USA.
Scott AlperDepartment of Biomedical Research and Center for Genes, Environment, and Health, National Jewish Health, University of Colorado, 1400 Jackson Street, Denver, CO, 80206, USA. alpers@njhealth.org.
Hong Wei ChuDepartment of Medicine, National Jewish Health, 1400 Jackson Street, Room A639, Denver, CO, 80206, USA. chuhw@njhealth.org.
National Jewish Health · USUniversity of Colorado Denver · US

Funding

Tollip inhibits IL-33 signaling during airway influenza virus infectionU19AI125357 · NIAID · UNIVERSITY OF ARIZONA · PI CHU, HONG W · 2016 to 2025
$14.7M
IRAK-M in lung defense against rhinovirus infectionR01AI106287 · NIAID · NATIONAL JEWISH HEALTH · PI CHU, HONG W, LI, LIWU · 2014 to 2018
$2.0M
SPLUNC1 in Severe AsthmaR01HL125128 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHU, HONG W, DI, YUANPU PETER · 2015 to 2018
$1.9M
Toxin-induced alternative mRNA splicing in Toll-like receptor signaling pathwaysR01ES025161 · NIEHS · NATIONAL JEWISH HEALTH · PI ALPER, SCOTT · 2016 to 2020
$1.8M
Novel function of MUC18: amplification of inflammation in allergic lungsR01HL122321 · NHLBI · NATIONAL JEWISH HEALTH · PI CHU, HONG W · 2015 to 2018
$1.6M
NIAID NIH HHS U19 AI125357NIEHS NIH HHS R01 ES025161NIH HHS 1R01 ES025161NIH HHS R01 AI106287NIH HHS R01 HL122321NIH HHS R01 HL125128NIH HHS U19AI125357,
6 · The paper itself

Abstract

backgroundAirway epithelial cells and alveolar macrophages (AMs) are the first line of defense in the lung during infection. Toll-like receptor (TLR) agonists have been extensively used to define the regulation of inflammation in these cells. However, previous studies were performed in non-paired airway epithelial cells and AMs. The major goal of our study was to compare the pro- and anti-inflammatory responses of paired human primary airway epithelial cells and AMs to TLR3 and TLR4 agonists.

methodsTracheobronchial epithelial cells (TBEC) and AMs from four smokers and four non-smokers without lung disease were cultured with or without Poly(I:C) (PIC) (a TLR3 agonist) or LPS (a TLR4 agonist) for 4, 24 and 48 h. The immune responses of paired cells were compared.

resultsTBEC and AMs showed stronger pro-inflammatory cytokine (e.g., IL-8) responses to PIC and LPS, respectively. TLR3 and TLR4 mRNA levels were similar in non-stimulated TBEC and AMs. However, PIC stimulation in AMs led to sustained up-regulation of the immune negative regulators Tollip and A20, which may render AMs less sensitive to PIC stimulation than TBEC. Unlike AMs, TBEC did not increase NF-κB activation after LPS stimulation. Interestingly, smoking status was correlated with less TLR3 and IRAK-M expression in non-stimulated TBEC, but not in AMs. PIC-stimulated TBEC and LPS-stimulated AMs from smokers vs. non-smokers produced more IL-8. Finally, we show that expression of A20 and IRAK-M is strongly correlated in the two paired cell types.

conclusionsBy using paired airway epithelial cells and AMs, this study reveals how these two critical types of lung cells respond to viral and bacterial pathogen associated molecular patterns, and provides rationale for modulating immune negative regulators to prevent excessive lung inflammation during respiratory infection.

Indexed as

AgedAnti-Inflammatory AgentsCells, CulturedFemaleHumansInflammationInflammation MediatorsMacrophages, AlveolarMaleMiddle AgedRespiratory MucosaSmokingAnti-Inflammatory AgentsInflammation MediatorsAlveolar macrophagesCigarette smokeImmune negative regulatorsInflammationPathogen associated molecular patternsToll-like receptorTracheobronchial epithelial cells

Identifiers

PMID29940963
PMCPMC6020222
OpenAlexW2810256275

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.