ArticleThe Journal of allergy and clinical immunology2018
Neonatal hyperoxia promotes asthma-like features through IL-33-dependent ILC2 responses.
Article in The Journal of allergy and clinical immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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.
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.
Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- Early life group 2 innate lymphoid cells in health and disease.Molecular and cellular pediatrics · 2026Review
- The IL-33-ILC2 axis: a key regulator of type 2 immunity in respiratory disease.Frontiers in immunology · 2026Review
- Intestinal IL-33 promotes microbiota-derived trimethylamine N -oxide synthesis and drives metabolic dysfunction-associated steatotic liver disease progression by exerting dual regulation on HIF-1α.Hepatology (Baltimore, Md.) · 2025Article
- Persistent B Cell-Derived MHC Class II Signaling Is Required for the Optimal Maintenance of Tissue-Resident Helper T Cells.ImmunoHorizons · 2024Article
- Establishment of a juvenile mouse asthma model induced by postnatal hyperoxia exposure combined with early OVA sensitization.Heliyon · 2024Article
- [Changes and significance of type 2 innate lymphoid cells and their related factors in bronchopulmonary dysplasia].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2023Article
- Effects of early postnatal hyperoxia exposure combined with early ovalbumin sensitization on lung inflammation and bacterial flora in a juvenile mouse model of asthma.Frontiers in microbiology · 2023Article
- Respiratory Follow Up of the Premature Neonates-Rationale and Practical Issues.Journal of clinical medicine · 2022Review
- Deficiency of endothelial FGFR1 alleviates hyperoxia-induced bronchopulmonary dysplasia in neonatal mice.Frontiers in pharmacology · 2022Article
- Inhaled Pharmacotherapy for Neonates: A Narrative Review.Turkish archives of pediatrics · 2022Article
- Review
- Roles of innate lymphoid cells (ILCs) in allergic diseases: The 10-year anniversary for ILC2s.The Journal of allergy and clinical immunology · 2021Review
- Characterization of the innate immune response in a novel murine model mimicking bronchopulmonary dysplasia.Pediatric research · 2021Article
- Immunization with anti-Tn immunogen in maternal rats protects against hyperoxia-induced kidney injury in newborn offspring.Pediatric research · 2021Article
- Tissue-resident CD4Science immunology · 2021Article
- Anti-Tn Monoclonal Antibody Ameliorates Hyperoxia-Induced Kidney Injury by Suppressing Oxidative Stress and Inflammation in Neonatal Mice.Mediators of inflammation · 2021Article
- The Fate of Activated Group 2 Innate Lymphoid Cells.Frontiers in immunology · 2021Review
- Article
- The immunological link between neonatal lung and eye disease.Clinical & translational immunology · 2021Review
- Type 2 Innate Lymphoid Cells Accumulate in the Brain After Hypoxia-Ischemia but Do Not Contribute to the Development of Preterm Brain Injury.Frontiers in cellular neuroscience · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundPremature infants often require oxygen supplementation and, therefore, are exposed to oxidative stress. Following oxygen exposure, preterm infants frequently develop chronic lung disease and have a significantly increased risk of asthma.
objectiveWe sought to identify the underlying mechanisms by which neonatal hyperoxia promotes asthma development.
methodsMice were exposed to neonatal hyperoxia followed by a period of room air recovery. A group of mice was also intranasally exposed to house dust mite antigen. Assessments were performed at various time points for evaluation of airway hyperresponsiveness, eosinophilia, mucus production, inflammatory gene expression, and T
resultsNeonatal hyperoxia induced asthma-like features including airway hyperresponsiveness, mucus hyperplasia, airway eosinophilia, and type 2 pulmonary inflammation. In addition, neonatal hyperoxia promoted allergic T
conclusionsThese data demonstrate that an axis involving IL-33 and ILC2s is important for the development of asthma-like features following neonatal hyperoxia and suggest therapeutic potential for targeting IL-33, ILC2s, and oxidative stress to prevent and/or treat asthma development related to prematurity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.