Evidence map›Paper›PMID 21695198›Full record

ArticlePloS one2011

Chlamydia pneumoniae infection induced allergic airway sensitization is controlled by regulatory T-cells and plasmacytoid dendritic cells.

Timothy R Crother, Nicolas W J Schröder, Justin Karlin, Shuang Chen, Kenichi Shimada, Anatoly Slepenkin, Randa Alsabeh, Ellena Peterson, Moshe Arditi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Microbiota and Immunity during Respiratory Infections: Lung and Gut Affair.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Forum on immunopathological diseases and therapeutics · 2016
    Article
  11. Inflammation and infections in asthma.The clinical respiratory journal · 2015
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. T cell-mediated host immune defenses in the lung.Annual review of immunology · 2013
    Review
  19. Article
  20. Respiratory syncytial virus vaccine development.Expert review of vaccines · 2011
    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

9 authors at 3 institutions in 1 country.

Timothy R CrotherPediatrics Infectious Diseases, Cedars-Sinai Medical Center, University of California Los Angeles, Los Angeles, California, United States of America.
Nicolas W J Schröder
Justin Karlin
Shuang Chen
Kenichi Shimada
Anatoly Slepenkin
Randa Alsabeh
Ellena Peterson
Moshe Arditi
Cedars-Sinai Medical Center · USUniversity of California, Los Angeles · USUniversity of California, Irvine · US

Funding

MOLECULAR PATHOGENESIS OF CHLAMYDIA-INDUCED ATHEROGENESIR01HL066436 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2001 to 2013
$3.6M
Role of Innate Immunity in Pathogenesis of Chlamydia Pneumonia InfectionR01AI067995 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2006 to 2010
$1.9M
Innate Immunity and Host Responses in Pathogenesis of Chlamydia PneumoniaeR56AI067995 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2012 to 2012
$413k
NHLBI NIH HHS HL-66436NHLBI NIH HHS R01 HL066436NIAID NIH HHS AI-067995NIAID NIH HHS R01 AI067995NIAID NIH HHS R56 AI067995
6 · The paper itself

Abstract

Chlamydia pneumoniae (CP) is associated with induction and exacerbation of asthma. CP infection can induce allergic airway sensitization in mice in a dose- and time-dependent manner. Allergen exposure 5 days after a low dose (mild-moderate), but not a high dose (severe) CP infection induces antigen sensitization in mice. Innate immune signals play a critical role in controlling CP infection induced allergic airway sensitization, however these mechanisms have not been fully elucidated. Wild-type, TLR2-/-, and TLR4-/- mice were infected intranasally (i.n.) with a low dose of CP, followed by i.n. exposure to human serum albumin (HSA) and challenged with HSA 2 weeks later. Airway inflammation, immunoglobulins, eosinophils, and goblet cells were measured. Low dose CP infection induced allergic sensitization in TLR2-/- mice, but not in TLR4-/- mice, due to differential Treg responses in these genotypes. TLR2-/- mice had reduced numbers of Tregs in the lung during CP infection while TLR4-/- mice had increased numbers. High dose CP infection resulted in an increase in Tregs and pDCs in lungs, which prevented antigen sensitization in WT mice. Depletion of Tregs or pDCs resulted in allergic airway sensitization. We conclude that Tregs and pDCs are critical determinants regulating CP infection-induced allergic sensitization. Furthermore, TLR2 and TLR4 signaling during CP infection may play a regulatory role through the modulation of Tregs.

Indexed as

ImmunizationAnimalsAntigens, BacterialBordetellaChlamydophila pneumoniaeDendritic CellsEosinophilsHumansInflammationLungLymphocyte DepletionMiceMicrobial ViabilityPneumonia, BacterialRespiratory HypersensitivitySerum AlbuminAntigens, BacterialSerum AlbuminTlr2 protein, mouseTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID21695198
PMCPMC3112152
OpenAlexW2069330688

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.