Evidence map›Paper›PMID 25465099›Full record

ArticleMucosal immunology2015

Distinct Tlr4-expressing cell compartments control neutrophilic and eosinophilic airway inflammation.

J W McAlees, G S Whitehead, I T W Harley, M Cappelletti, C L Rewerts, A M Holdcroft, S Divanovic, M Wills-Karp, F D Finkelman, C L Karp and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

61 citing papers in PubMed, 92 citations in OpenAlex.

  1. Trial
  2. Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Molecular Study from the Signaling Pathways of Four PotentialInternational journal of molecular sciences · 2025
    Article
  8. Review
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1 more citing papers are in PubMed but not listed here.

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 1 country.

J W McAleesDivision of Immunobiology, Cincinnati Children's Hospital Research Foundation, Cincinnati, Ohio, USA.
G S WhiteheadLaboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
I T W HarleyDivision of Immunobiology, Cincinnati Children's Hospital Research Foundation, Cincinnati, Ohio, USA.
M CappellettiDivision of Immunobiology, Cincinnati Children's Hospital Research Foundation, Cincinnati, Ohio, USA.
C L RewertsDivision of Immunobiology, Cincinnati Children's Hospital Research Foundation, Cincinnati, Ohio, USA.
A M HoldcroftDivision of Immunobiology, Cincinnati Children's Hospital Research Foundation, Cincinnati, Ohio, USA.
S DivanovicDivision of Immunobiology, Cincinnati Children's Hospital Research Foundation, Cincinnati, Ohio, USA.
M Wills-Karp1] Division of Immunobiology, Cincinnati Children's Hospital Research Foundation, Cincinnati, Ohio, USA [2] Present address: Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
F D Finkelman1] Division of Immunobiology, Cincinnati Children's Hospital Research Foundation, Cincinnati, Ohio, USA [2] Department of Medicine, Cincinnati Veterans Affairs Medical Center, Cincinnati, Ohio, USA [3] Department of Internal Medicine, Division of Allergy, Immunology and Rheumatology, University of Cincinnati School of Medicine, Cincinnati, Ohio, USA.
C L Karp1] Division of Immunobiology, Cincinnati Children's Hospital Research Foundation, Cincinnati, Ohio, USA [2] Bill & Melinda Gates Foundation, Seattle, WA, USA.
D N CookLaboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
Cincinnati Children's Hospital Medical Center · USNational Institute of Environmental Health Sciences · USBill & Melinda Gates Foundation · USJohns Hopkins University · US

Funding

Allergic sensitization through the airwayZIAES102025 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI COOK, DONALD N · 2009 to 2025
$32.6M
Molecular Genetics Support to Identify Gene/Environment Interactions in DiseaseZICES102546 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI GERRISH, KEVIN · 2009 to 2025
$30.5M
Allergenicity resulting from functional mimicry of the TLR complexR01AI088372 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI FINKELMAN, FRED DOUGLASS · 2010 to 2014
$1.9M
Immunobiology of IFRD1, a gene modifying CF lung diseaseR01HL094576 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI HOEBE, KASPER · 2009 to 2012
$1.5M
Der p 2-driven TLR4 signaling in allergic asthmaF32HL110497 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI MCALEES, JACLYN W · 2011 to 2013
$67k
Intramural NIH HHS ZIA ES102025NHLBI NIH HHS F32 HL110497NHLBI NIH HHS R01 HL094576NIAID NIH HHS R01 AI088372
6 · The paper itself

Abstract

Allergic asthma is a chronic, inflammatory lung disease. Some forms of allergic asthma are characterized by T helper type 2 (Th2)-driven eosinophilia, whereas others are distinguished by Th17-driven neutrophilia. Stimulation of Toll-like receptor 4 (TLR4) on hematopoietic and airway epithelial cells (AECs) contributes to the inflammatory response to lipopolysaccharide (LPS) and allergens, but the specific contribution of TLR4 in these cell compartments to airway inflammatory responses remains poorly understood. We used novel, conditionally mutant Tlr4(fl/fl) mice to define the relative contributions of AEC and hematopoietic cell Tlr4 expression to LPS- and allergen-induced airway inflammation. We found that Tlr4 expression by hematopoietic cells is critical for neutrophilic airway inflammation following LPS exposure and for Th17-driven neutrophilic responses to the house dust mite (HDM) lysates and ovalbumin (OVA). Conversely, Tlr4 expression by AECs was found to be important for robust eosinophilic airway inflammation following sensitization and challenge with these same allergens. Thus, Tlr4 expression by hematopoietic and airway epithelial cells controls distinct arms of the immune response to inhaled allergens.

Indexed as

Gene ExpressionAnimalsAsthmaCytokinesDendritic CellsDisease Models, AnimalEosinophilsEpithelial CellsImmunity, InnateLipopolysaccharidesLungMiceMice, KnockoutNeutrophilsPyroglyphidaeRespiratory MucosaCytokinesLipopolysaccharidesToll-Like Receptor 4

Identifiers

PMID25465099
PMCPMC4454628
OpenAlexW2041747140

What OpenQuestion holds

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LicenceTDM
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.