Evidence map›Paper›PMID 19661246›Full record

ArticleAmerican journal of respiratory and critical care medicine2009

Allergic sensitization through the airway primes Th17-dependent neutrophilia and airway hyperresponsiveness.

Rhonda H Wilson, Gregory S Whitehead, Hideki Nakano, Meghan E Free, Jay K Kolls, Donald N Cook

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 221 papers.

0numbers the graph read from it
0cells of the map it votes in
221citing papers in PubMed
16.9field-weighted citation impact, top 1% 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

221 citing papers in PubMed, 399 citations in OpenAlex.

  1. Trial
  2. Distinct miRNA expression patterns in circulating eosinophil subtypes and their subtype-derived exosomes in allergic asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
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  9. Asthma Phenotypes and Biomarkers.Respiratory care · 2025
    Review
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  15. Review
  16. Article
  17. Review
  18. Article
  19. Elevated Proportions of Circulating CXCR5Journal of immunology research · 2024
    Article
  20. Review

161 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

6 authors at 3 institutions in 1 country.

Rhonda H WilsonDivision of Intramural Research, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709, USA.
Gregory S Whitehead
Hideki Nakano
Meghan E Free
Jay K Kolls
Donald N Cook
National Institutes of Health · USNational Institute of Environmental Health Sciences · USUniversity of Pittsburgh · US

Funding

Allergic sensitization through the airwayZIAES102025 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI COOK, DONALD N · 2009 to 2025
$32.6M
genetic requirements of allergic responses in the lungZ01ES102025 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI COOK, DONALD N · 2006 to 2008
$3.4M
Intramural NIH HHS
6 · The paper itself

Abstract

rationaleIn humans, immune responses to inhaled aeroallergens develop in the lung and draining lymph nodes. Many animal models of asthma bypass this route and instead use intraperitoneal injections of allergen using aluminum hydroxide as an adjuvant.

objectivesWe investigated whether allergic sensitization through the airway elicits immune responses qualitatively different than those arising in the peritoneum.

methodsMice were sensitized to allergen through the airway using low-dose LPS as an adjuvant, or through the peritoneum using aluminum hydroxide as an adjuvant. After a single allergen challenge, ELISA and flow cytometry were used to measure cytokines and leukocyte subsets. Invasive measurements of airway resistance were used to measure allergen-induced airway hyperreactivity (AHR). MEASUREMENTS AND MAIN

resultsSensitization through the peritoneum primed strong Th2 responses and eosinophilia, but not AHR, after a single allergen challenge. By contrast, allergic sensitization through the airway primed only modest Th2 responses, but strong Th17 responses. Th17 cells homed to the lung and released IL-17 into the airway on subsequent encounter with inhaled allergen. As a result, these mice developed IL-17-dependent airway neutrophilia and AHR. This AHR was neutrophil-dependent because it was abrogated in CXCR2-deficient mice and also in wild-type mice receiving a neutrophil-depleting antibody. Individually, neither IL-17 nor ongoing Th2 responses were sufficient to confer AHR, but together they acted synergistically to promote neutrophil recruitment, eosinophil recruitment and AHR.

conclusionsAllergic sensitization through the airway primes modest Th2 responses but strong Th17 responses that promote airway neutrophilia and acute AHR. These findings support a causal role for neutrophils in severe asthma.

Indexed as

Disease Models, AnimalAnimalsAsthmaBronchial HyperreactivityImmunizationInterleukin-17LeukocytosisLipopolysaccharidesMiceMice, Inbred BALB CMice, KnockoutNeutrophilsT-Lymphocyte SubsetsInterleukin-17Lipopolysaccharides

Identifiers

PMID19661246
PMCPMC2778149
OpenAlexW1972025293

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.