Evidence map›Paper›PMID 24023674›Full record

ArticlePloS one2013

TLR2 regulates neutrophil recruitment and cytokine production with minor contributions from TLR9 during hypersensitivity pneumonitis.

Kelly Andrews, Hossam Abdelsamed, Ae-Kyung Yi, Mark A Miller, Elizabeth A Fitzpatrick

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. How experimental models have unlocked hidden mechanisms of hypersensitivity pneumonitis.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Muc5b plays a role in the development of inflammation and fibrosis in hypersensitivity pneumonitis induced byAmerican journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  8. Differential Gene Sets Profiling in Gram-Negative and Gram-Positive Sepsis.Frontiers in cellular and infection microbiology · 2022
    Article
  9. Review
  10. Article
  11. Article
  12. S1PAmerican journal of respiratory cell and molecular biology · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. A critical role of Dectin-1 in hypersensitivity pneumonitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    Article
  20. 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

5 authors at 1 institution in 1 country.

Kelly AndrewsDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, Tennessee, United States of America.
Hossam Abdelsamed
Ae-Kyung Yi
Mark A Miller
Elizabeth A Fitzpatrick
University of Tennessee Health Science Center · US

Funding

Induction of immunological paralysis by CpG DNAR01AI053137 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI YI, AE-KYUNG · 2004 to 2008
$1.4M
The Role of Neutrophils in Hypersensitivity PneumonitisR01HL084172 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI FITZPATRICK, ELIZABETH ANN · 2007 to 2010
$1.3M
NHLBI NIH HHS HL084172NHLBI NIH HHS R01 HL084172NIAID NIH HHS R01 AI053137
6 · The paper itself

Abstract

Hypersensitivity pneumonitis (HP) is an interstitial lung disease that develops following repeated exposure to environmental antigens. The disease results in alveolitis, granuloma formation and may progress to a fibrotic chronic form, which is associated with significant morbidity and mortality. The severity of the disease correlates with a neutrophil rich influx and an IL-17 response. We used the Saccharopolysporarectivirgula (SR) model of HP to determine whether Toll-like receptors (TLR) 2 and 9 cooperate in neutrophil recruitment and IL-17-associated cytokine production during the development of HP. Stimulation of bone marrow derived macrophages (BMDMs) from C57BL/6, MyD88(-/-) and TLR2/9(-/-) mice with SR demonstrate that SR is a strong inducer of neutrophil chemokines and growth factors. The cytokines induced by SR were MyD88-dependent and, of those, most were partially or completely dependent on TLRs 2 and 9. Following in vivo exposure to SR, CXCL2 production and neutrophil recruitment were reduced in TLR2(-/-) and TLR2/9(-/-) mice suggesting that the response was largely dependent on TLR2; however the reduction was greatest in the TLR2/9(-/-) double knockout mice indicating TLR9 may also contribute to the response. There was a reduction in the levels of pro-inflammatory cytokines TNFα and IL-6 as well as CCL3 and CCL4 in the BALF from TLR2/9(-/-) mice compared to WT and single knockout (SKO) mice exposed one time to SR. The decrease in neutrophil recruitment and TNFα production in the TLR2/9(-/-) mice was maintained throughout 3 weeks of SR exposures in comparison to WT and SKO mice. Both TLRs 2 and 9 contributed to the Th17 response; there was a decrease in Th17 cells and IL-17 mRNA in the TLR2/9(-/-) mice in comparison to the WT and SKO mice. Despite the effects on neutrophil recruitment and the IL-17 response, TLR2/9(-/-) mice developed granuloma formation similarly to WT and SKO mice suggesting that there are additional mediators and pattern recognition receptors involved in the disease.

Indexed as

Alveolitis, Extrinsic AllergicAnimalsChemokinesCytokinesFemaleGranulomaInflammationLungLymphocytesMacrophagesMiceMice, Inbred C57BLMutationNeutrophil InfiltrationSaccharopolysporaTh17 CellsChemokinesCytokinesTlr2 protein, mouseTlr9 protein, mouseToll-Like Receptor 2Toll-Like Receptor 9

Identifiers

PMID24023674
PMCPMC3758260
OpenAlexW2058588911

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.