Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (681 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Tendency of the smooth muscle of the tracheobronchial tree to contract more intensely in response to a given stimulus than it does in the response seen in normal individuals. This condition is present in virtually all symptomatic patients with asthma. The most prominent manifestation of this smooth muscle contraction is a decrease in airway caliber that can be readily measured in the pulmonary function laboratory.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Bronchial Hyperreactivities; Hyperreactivities, Bronchial; Hyperreactivity, Bronchial.
Where it fits in the MeSH classification
- Broader topics
- Bronchial Diseases
- See also
- Asthma
Research landscape
PubMed indexes 7,623 records tagged with the MeSH heading “Bronchial Hyperreactivity” (counts retrieved 2026-11-04). 267 of them (3.5%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 3,161 records.
Reviews account for 1,147 records (15.0%) and meta-analyses for 25. Randomized controlled trials number 473 (6.2%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 2,494 |
| 2000-2009 | 3,161 |
| 2010-2019 | 1,701 |
| 2020 onward | 267 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,147 | 15.0% |
| Meta-analyses | 25 | 0.3% |
| Randomized controlled trials | 473 | 6.2% |
Method: PubMed query "Bronchial Hyperreactivity"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in respiratory medicine
Research on airway and lung disease mixes lung-function tests, symptom diaries, imaging and hospital records, so what was measured and in whom matters as much as the result. Many conditions here, such as asthma and COPD, vary between people and over time, and exposure studies (smoking, pollution, workplace dust) show association rather than proof of cause. Nothing on this page is advice about treatment or inhalers; anyone with breathing difficulty should seek care from a qualified clinician. Check how the condition was defined, the severity of the people studied and whether outcomes were symptoms, lung function or hospital admissions.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Critical role of actin-associated proteins in smooth muscle contraction, cell proliferation, airway hyperresponsiveness and airway remodeling | 2015 | Review article Design not recorded in structured metadata | 90 | cc by PMID 26517982 · DOI · PMC4628321 |
| Brainstem Dbh+ neurons control allergen-induced airway hyperreactivity | 2024 | Research article Design not recorded in structured metadata | 77 | cc by PMID 38987587 · DOI · PMC11254774 |
| A 4-Week Model of House Dust Mite (HDM) Induced Allergic Airways Inflammation with Airway Remodeling | 2018 | Research article Design not recorded in structured metadata | 73 | cc by PMID 29720689 · DOI · PMC5932037 |
| Sex and the Developmental Environment Shape Molecular Networks Underlying Bronchial Responsiveness in Mice | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 41665211 · DOI · PMC12888530 |
Critical role of actin-associated proteins in smooth muscle contraction, cell proliferation, airway hyperresponsiveness and airway remodeling [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Asthma is characterized by airway hyperresponsiveness and airway remodeling, which are largely attributed to increased airway smooth muscle contractility and cell proliferation.
- Closing excerpt
- These studies indicate that Abl may be a novel target for the development of new therapy to treat asthma.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (138 words)
Asthma is characterized by airway hyperresponsiveness and airway remodeling, which are largely attributed to increased airway smooth muscle contractility and cell proliferation. It is known that both chemical and mechanical stimulation regulates smooth muscle contraction. Recent studies suggest that contractile activation and mechanical stretch induce actin cytoskeletal remodeling in smooth muscle. However, the mechanisms that control actin cytoskeletal reorganization are not completely elucidated. This review summarizes our current understanding regarding how actin-associated proteins may regulate remodeling of the actin cytoskeleton in airway smooth muscle. In particular, there is accumulating evidence to suggest that Abelson tyrosine kinase (Abl) plays a critical role in regulating airway smooth muscle contraction and cell proliferation in vitro, and airway hyperresponsiveness and remodeling in vivo. These studies indicate that Abl may be a novel target for the development of new therapy to treat asthma.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26517982 · DOI · PMC4628321
Brainstem Dbh+ neurons control allergen-induced airway hyperreactivity [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Exaggerated airway constriction triggered by repeated exposure to allergen, also called hyperreactivity, is a hallmark of asthma.
- Closing excerpt
- This knowledge informs how neural modulation could be used to control allergen-induced airway hyperreactivity.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (199 words)
Exaggerated airway constriction triggered by repeated exposure to allergen, also called hyperreactivity, is a hallmark of asthma. Whereas vagal sensory neurons are known to function in allergen-induced hyperreactivity1-3, the identity of downstream nodes remains poorly understood. Here we mapped a full allergen circuit from the lung to the brainstem and back to the lung. Repeated exposure of mice to inhaled allergen activated the nuclei of solitary tract (nTS) neurons in a mast cell-, interleukin-4 (IL-4)- and vagal nerve-dependent manner. Single-nucleus RNA sequencing, followed by RNAscope assay at baseline and allergen challenges, showed that a Dbh+ nTS population is preferentially activated. Ablation or chemogenetic inactivation of Dbh+ nTS neurons blunted hyperreactivity whereas chemogenetic activation promoted it. Viral tracing indicated that Dbh+ nTS neurons project to the nucleus ambiguus (NA) and that NA neurons are necessary and sufficient to relay allergen signals to postganglionic neurons that directly drive airway constriction. Delivery of noradrenaline antagonists to the NA blunted hyperreactivity, suggesting noradrenaline as the transmitter between Dbh+ nTS and NA. Together, these findings provide molecular, anatomical and functional definitions of key nodes of a canonical allergen response circuit. This knowledge informs how neural modulation could be used to control allergen-induced airway hyperreactivity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38987587 · DOI · PMC11254774
A 4-Week Model of House Dust Mite (HDM) Induced Allergic Airways Inflammation with Airway Remodeling [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Animal models of allergic airways inflammation are useful tools in studying the pathogenesis of asthma and potential therapeutic interventions.
- Closing excerpt
- We conclude that this new 4-week HDM model is another useful tool in studies of human asthma that offers advantages of shorter duration for development and decreased costs when compared to other models that require longer durations of exposure (5-12 weeks) to develop.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (201 words)
Animal models of allergic airways inflammation are useful tools in studying the pathogenesis of asthma and potential therapeutic interventions. The different allergic airways inflammation models available to date employ varying doses, frequency, duration and types of allergen, which lead to the development of different features of asthma; showing varying degrees of airways inflammation and hyper-responsiveness (AHR) and airways remodeling. Models that also exhibit airway remodeling, a key feature of asthma, in addition to AHR and airway inflammation typically require 5-12 weeks to develop. In this report, we describe a 4-week mouse model of house dust mite (HDM)-induced allergic airways inflammation, and compare the phenotypic features of two different doses of HDM exposures (10 µg and 25 µg) for 5 days/week with a well-characterized 8-week chronic HDM model. We found that 4 weeks of intranasal HDM (25 µg in 35 µl saline; 5 days/week) resulted in AHR, airway inflammation and airway remodeling that were comparable to the 8-week model. We conclude that this new 4-week HDM model is another useful tool in studies of human asthma that offers advantages of shorter duration for development and decreased costs when compared to other models that require longer durations of exposure (5-12 weeks) to develop.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29720689 · DOI · PMC5932037
Sex and the Developmental Environment Shape Molecular Networks Underlying Bronchial Responsiveness in Mice [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Epidemiological evidence supports sex-specific prevalence patterns of respiratory disease, yet the molecular basis of these dimorphic patterns under normal physiological conditions remains poorly understood.
- Closing excerpt
- These findings provide new insight into the molecular architecture of sex-based differences in lung function and highlight the importance of incorporating both sex and developmental context in respiratory research.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (143 words)
Epidemiological evidence supports sex-specific prevalence patterns of respiratory disease, yet the molecular basis of these dimorphic patterns under normal physiological conditions remains poorly understood. Using an isogenic murine model, we assessed bronchial responsiveness to methacholine in male and female adult offspring, with and without maternal exposure to air pollution particulates. We confirmed that males exhibit significantly greater bronchial responsiveness than females, independent of maternal exposure. RNA sequencing of lung tissue, coupled with gene co-expression analysis, revealed differentially expressed genes and sex-specific gene network modules associated with this physiological dimorphism. Interestingly, although maternal exposure did not alter the physiological response, it did interact with sex to affect which gene modules are associated with bronchial responsiveness. These findings provide new insight into the molecular architecture of sex-based differences in lung function and highlight the importance of incorporating both sex and developmental context in respiratory research.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41665211 · DOI · PMC12888530
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Guidelines for methacholine and exercise challenge testing-1999. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, July 1999 [5]
- Research article Mechanisms of airway hyperresponsiveness [6]
- Research article Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma [7]
- Research article Asthma remission: what is it and how can it be achieved? [8]
- Research article Virus-induced airway hyperresponsiveness and asthma [9]
- Research article Specific inhalation challenge in the diagnosis of occupational asthma: consensus statement [10]
References
- Tang DD. Critical role of actin-associated proteins in smooth muscle contraction, cell proliferation, airway hyperresponsiveness and airway remodeling. . 2015. PMID 26517982 · DOI · PMC4628321
- Su Y, Xu J, Zhu Z, Chin J, Xu L, Yu H, et al.. Brainstem Dbh+ neurons control allergen-induced airway hyperreactivity. . 2024. PMID 38987587 · DOI · PMC11254774
- Woo LN, Guo WY, Wang X, Young A, Salehi S, Hin A, et al.. A 4-Week Model of House Dust Mite (HDM) Induced Allergic Airways Inflammation with Airway Remodeling. . 2018. PMID 29720689 · DOI · PMC5932037
- Zakarya R, Wang B, Chan YL, Xenaki D, Ho KF, Guo H, et al.. Sex and the Developmental Environment Shape Molecular Networks Underlying Bronchial Responsiveness in Mice. . 2026. PMID 41665211 · DOI · PMC12888530
- Crapo RO, Casaburi R, Coates AL, Enright PL, Hankinson JL, Irvin CG, et al.. Guidelines for methacholine and exercise challenge testing-1999. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, July 1999. Am J Respir Crit Care Med. 2000. PMID 10619836 · DOI
- Cockcroft DW, Davis BE. Mechanisms of airway hyperresponsiveness. J Allergy Clin Immunol. 2006. PMID 16950269 · DOI
- An SS, Bai TR, Bates JH, Black JL, Brown RH, Brusasco V, et al.. Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma. Eur Respir J. 2007. PMID 17470619 · DOI · PMC2527453
- Thomas D, McDonald VM, Pavord ID, Gibson PG. Asthma remission: what is it and how can it be achieved?. Eur Respir J. 2022. PMID 35361633 · DOI · PMC9630609
- Folkerts G, Busse WW, Nijkamp FP, Sorkness R, Gern JE. Virus-induced airway hyperresponsiveness and asthma. Am J Respir Crit Care Med. 1998. PMID 9620896 · DOI
- Vandenplas O, Suojalehto H, Aasen TB, Baur X, Burge PS, de Blay F, et al.. Specific inhalation challenge in the diagnosis of occupational asthma: consensus statement. Eur Respir J. 2014. PMID 24603815 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.