Evidence map›Paper›PMID 22042134›Full record

ArticleJournal of innate immunity2012

Heat shock factor 1 protects against lung mycoplasma pneumoniae infection in mice.

Fabienne Gally, Maisha N Minor, Sean K Smith, Stephanie R Case, Hong Wei Chu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of innate immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

17 citing papers in PubMed, 16 citations in OpenAlex.

  1. Nutrients · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Immune dysregulation inFrontiers in immunology · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. A role for heat shock factor 1 in hypercapnia-induced inhibition of inflammatory cytokine expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  12. Article
  13. Review
  14. [Effect of heat shock factor 1 on airway hyperresponsiveness and airway inflammation in mice with allergic asthma].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2017
    Article
  15. Article
  16. Article
  17. 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 2 institutions in 1 country.

Fabienne GallyDepartment of Medicine, National Jewish Health, Denver, CO, USA.
Maisha N Minor
Sean K Smith
Stephanie R Case
Hong Wei Chu
University of Colorado Denver · USNational Jewish Health · US

Funding

SPLUNC1 protein in host defense against Mycoplasma pneumoniae infectionR01HL088264 · NHLBI · NATIONAL JEWISH HEALTH · PI CHU, HONG W · 2009 to 2012
$1.8M
Effects of Allergic Inflammation on TLR2 Signaling and Mycoplasma InfectionR01AI070175 · NIAID · NATIONAL JEWISH HEALTH · PI CHU, HONG W · 2008 to 2011
$1.6M
NHLBI NIH HHS R01 HL088264NIAID NIH HHS R01 AI070175
6 · The paper itself

Abstract

Heat shock factor 1 (HSF1) is a transcriptional factor that controls the induction of heat shock proteins (e.g. HSP70) in response to stress. Bacterial infections contribute to the pathobiology of chronic lung diseases such as chronic obstructive pulmonary disease and asthma. Whether HSF1 is critical to lung bacterial infection remains unknown. This study is aimed at investigating the impact of HSF1 deficiency on lung Mycoplasma pneumoniae (Mp) infection and elucidating the underlying molecular mechanisms, such as Toll-like receptor 2 (TLR2) signaling. HSF1(-/-) and HSF1(+/+) mice were intranasally infected with Mp or saline and sacrificed 4, 24 and 72 h after treatment. HSF1(-/-) mice had a higher lung Mp load than HSF1(+/+) mice. Mp-induced lung TLR2, nuclear factor-κB and associated inflammation [e.g. keratinocyte-derived chemokine (KC), neutrophils and histopathology] were delayed in HSF1(-/-) mice as compared to HSF1(+/+) mice. HSP70 protein levels in bronchoalveolar lavage fluid of HSF1(-/-) mice were decreased. Furthermore, in response to Mp infection, HSF1(-/-) alveolar macrophages had less TLR2 mRNA expression and KC production than HSF1(+/+) counterparts. Nuclear factor-κB activity and KC production in HSF1(-/-) macrophages could be rescued by addition of exogenous HSP70 protein. These data suggest that HSF1 is necessary to initiate host defense against bacterial infection partly through promoting early TLR2 signaling activation.

Indexed as

Immunity, InnateAnimalsBronchoalveolar LavageDNA-Binding ProteinsHeat Shock Transcription FactorsHSP70 Heat-Shock ProteinsLungMacrophages, AlveolarMiceMice, KnockoutMycoplasma pneumoniaeNF-kappa BPneumonia, MycoplasmaSignal TransductionToll-Like Receptor 2Transcription FactorsDNA-Binding ProteinsHeat Shock Transcription FactorsHsf1 protein, mouseHSP70 Heat-Shock ProteinsNF-kappa BTlr2 protein, mouseToll-Like Receptor 2Transcription Factors

Identifiers

PMID22042134
PMCPMC3250656
OpenAlexW2038371679

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.