ArticleAmerican journal of respiratory cell and molecular biology2022
Unique Allergic Asthma Phenotypes in Offspring of House Dust Mite-exposed Mice.
Article in American journal of respiratory cell and molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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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.
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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.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Maternal asthma during pregnancy and risks of allergy and asthma in progeny: A systematic review and meta-analysis.BJOG : an international journal of obstetrics and gynaecology · 2025Pooled it
- Molecular mechanisms and therapeutic targets in lung cancer-nerve crosstalk.Chinese medical journal pulmonary and critical care medicine · 2026Review
- Parasympathetic Airway Hyperreactivity Is Enhanced in Acute but Not Chronic Eosinophilic Asthma Mouse Models.American journal of respiratory cell and molecular biology · 2025Article
- Maternal IgE Influence on Fetal and Infant Health.Immunological reviews · 2025Review
- Maternal asthma imprints fetal lung ILC2s via glucocorticoid signaling leading to worsened allergic airway inflammation in murine adult offspring.Nature communications · 2025Article
- The Prevention of House Dust Mite Allergies in Pediatric Asthma.Children (Basel, Switzerland) · 2024Review
- Preclinical models of maternal asthma and progeny outcomes: a scoping review.European respiratory review : an official journal of the European Respiratory Society · 2024Article
- Review
- Grandmaternal allergen sensitization reprograms epigenetic and airway responses to allergen in second-generation offspring.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- DOCK2 Promotes Asthma Development by Eliciting Airway Epithelial-Mesenchymal Transition.American journal of respiratory cell and molecular biology · 2023Article
- Maternal Allergen Exposures and Development of Asthma: Kids Are Airways Nervy.American journal of respiratory cell and molecular biology · 2022Article
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6 authors at 2 institutions in 1 country.
Funding
Abstract
Asthma is a heterogeneous inflammatory airway disease that develops in response to a combination of genetic predisposition and environmental exposures. Patients with asthma are grouped into phenotypes with shared clinical features and biomarker profiles to help tailor specific therapies. However, factors driving development of specific phenotypes are poorly understood. Prenatal exposure to maternal asthma is a unique risk factor for childhood asthma. Here we tested whether maternal asthma skews asthma phenotypes in offspring. We compared airway hyperreactivity and inflammatory and neurotrophin lung signatures before and after allergen challenge in offspring born to mice exposed to house dust mite (HDM) or vehicle during pregnancy. Maternal HDM exposure potentiated offspring responses to HDM allergen, significantly increasing both airway hyperreactivity and airway eosinophilia compared with control mice. Maternal HDM exposure broadly skewed the offspring cytokine response from a classic allergen-induced T-helper cell type 2 (Th2)-predominant signature in HDM-treated offspring of vehicle-exposed mothers, toward a mixed Th17/Th1 phenotype in HDM-treated offspring of HDM-exposed mothers. Morphologic analysis determined that maternal HDM exposure also increased airway epithelial sensory nerve density and induced distinct neurotrophin signatures to support airway hyperinnervation. Our results demonstrate that maternal allergen exposure alters fetal lung development and promotes a unique inflammatory phenotype at baseline and in response to allergen that persists into adulthood.
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