ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Maternal exposure to secondhand cigarette smoke primes the lung for induction of phosphodiesterase-4D5 isozyme and exacerbated Th2 responses: rolipram attenuates the airway hyperreactivity and muscarinic receptor expression but not lung inflammation and atopy.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 56 citations in OpenAlex.
- Prenatal Cannabis and Tobacco: Studies in Animal Models.Advances in experimental medicine and biology · 2026Review
- Cyclic nucleotide phosphodiesterases as drug targets.Pharmacological reviews · 2025Review
- Morpho-molecular and nutritional profiling for yield improvement and value addition of indigenous aromatic Joha rice of Assam.Scientific reports · 2024Article
- Early-life exposure to cigarette smoke primes lung function and DNA methylation changes atAmerican journal of physiology. Lung cellular and molecular physiology · 2023Article
- Investigation on Nutritional, Phytochemical, and Antioxidant Abilities of Various Traditional Rice Varieties.Applied biochemistry and biotechnology · 2023Article
- Keratinocytes-Derived Reactive Oxygen Species Play an Active Role to Induce Type 2 Inflammation of the Skin: A Pathogenic Role of Reactive Oxygen Species at the Early Phase of Atopic Dermatitis.Annals of dermatology · 2021Article
- Article
- Cigarette Smoking Modulation of Saliva Microbial Composition and Cytokine Levels.International journal of environmental research and public health · 2018Article
- The prevention of 2,4-dinitrochlorobenzene-induced inflammation in atopic dermatitis-like skin lesions in BALB/c mice by Jawoongo.BMC complementary and alternative medicine · 2018Article
- Cigarette smoke up-regulates PDE3 and PDE4 to decrease cAMP in airway cells.British journal of pharmacology · 2018Article
- Epigenetics of Mucus Hypersecretion in Chronic Respiratory Diseases.American journal of respiratory cell and molecular biology · 2018Review
- α7 nAChR mediated Fas demethylation contributes to prenatal nicotine exposure-induced programmed thymocyte apoptosis in mice.Oncotarget · 2017Article
- Prenatal tobacco smoke exposure predisposes offspring mice to exacerbated allergic airway inflammation associated with altered innate effector function.Particle and fibre toxicology · 2017Article
- Sex-specific lung functional changes in adult mice exposed only to second-hand smoke in utero.Respiratory research · 2017Article
- Gestational Exposure to Sidestream (Secondhand) Cigarette Smoke Promotes Transgenerational Epigenetic Transmission of Exacerbated Allergic Asthma and Bronchopulmonary Dysplasia.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Review
- Prenatal nicotinic exposure augments cardiorespiratory responses to activation of bronchopulmonary C-fibers.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Inter- and transgenerational epigenetic inheritance: evidence in asthma and COPD?Clinical epigenetics · 2015Article
- In Utero Cigarette Smoke Affects Allergic Airway Disease But Does Not Alter the Lung Methylome.PloS one · 2015Article
- HIF-1α Plays a Critical Role in the Gestational Sidestream Smoke-Induced Bronchopulmonary Dysplasia in Mice.PloS one · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Airway hyperreactivity (AHR), lung inflammation, and atopy are clinical signs of allergic asthma. Gestational exposure to cigarette smoke (CS) markedly increases the risk for childhood allergic asthma. Muscarinic receptors regulate airway smooth muscle tone, and asthmatics exhibit increased AHR to muscarinic agonists. We have previously reported that in a murine model of bronchopulmonary aspergillosis, maternal exposure to mainstream CS increases AHR after acute intratracheal administration of Aspergillus fumigatus extract. However, the mechanism by which gestational CS induces allergic asthma is unclear. We now show for the first time that, compared with controls, mice exposed prenatally to secondhand CS exhibit increased lung inflammation (predominant infiltration by eosinophils and polymorphs), atopy, and airway resistance, and produce proinflammatory cytokines (IL-4, IL-5, IL-6, and IL-13, but not IL-2 or IFN-gamma). These changes, which occur only after an allergen (A. fumigatus extract) treatment, are correlated with marked up-regulated lung expression of M1, M2, and M3 muscarinic receptors and phosphodiesterase (PDE)4D5 isozyme. Interestingly, the PDE4-selective inhibitor rolipram attenuates the increase in AHR, muscarinic receptors, and PDE4D5, but fails to down-regulate lung inflammation, Th2 cytokines, or serum IgE levels. Thus, the fetus is extraordinarily sensitive to CS, inducing allergic asthma after postnatal exposure to allergens. Although the increased AHR might reflect increased PDE4D5 and muscarinic receptor expression, the mechanisms underlying atopy and lung inflammation are unrelated to the PDE4 activity. Thus, PDE4 inhibitors might ease AHR, but are unlikely to attenuate lung inflammation and atopy associated with childhood allergic asthma.
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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.