ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Airway responsiveness in CD38-deficient mice in allergic airway disease: studies with bone marrow chimeras.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Hematopoietic 12/15-lipoxygenase activity negatively contributes to fungal-associated allergic asthma.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Lymphocyte Subsets and Pulmonary Nodules to Predict the Progression of Sarcoidosis.Biomedicines · 2023Article
- Aging-Related Mechanisms Contribute to Corticosteroid Insensitivity in Elderly Asthma.International journal of molecular sciences · 2023Review
- CD38 plays an age-related role in cholinergic deregulation of airway smooth muscle contractility.The Journal of allergy and clinical immunology · 2022Article
- CD38 deficiency alleviates Ang II-induced vascular remodeling by inhibiting small extracellular vesicle-mediated vascular smooth muscle cell senescence in mice.Signal transduction and targeted therapy · 2021Article
- Chitinase 3-like-1 protects airway function despite promoting type 2 inflammation during fungal-associated allergic airway inflammation.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- CD31Journal of thoracic disease · 2021Article
- Novel Pathway of Adenosine Generation in the Lungs from NADMolecules (Basel, Switzerland) · 2020Article
- Role of CD38/cADPR signaling in obstructive pulmonary diseases.Current opinion in pharmacology · 2020Review
- Edaravone attenuates experimental asthma in mice through induction of HO-1 and the Keap1/Nrf2 pathway.Experimental and therapeutic medicine · 2020Article
- Review
- CD38/cADPR Signaling Pathway in Airway Disease: Regulatory Mechanisms.Mediators of inflammation · 2018Review
- CD38 in the pathogenesis of allergic airway disease: Potential therapeutic targets.Pharmacology & therapeutics · 2017Review
- Emerging concepts in smooth muscle contributions to airway structure and function: implications for health and disease.American journal of physiology. Lung cellular and molecular physiology · 2016Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
CD38 is a cell-surface protein involved in calcium signaling and contractility of airway smooth muscle. It has a role in normal airway responsiveness and in airway hyperresponsiveness (AHR) developed following airway exposure to IL-13 and TNF-α but appears not to be critical to airway inflammation in response to the cytokines. CD38 is also involved in T cell-mediated immune response to protein antigens. In this study, we assessed the contribution of CD38 to AHR and inflammation to two distinct allergens, ovalbumin and the epidemiologically relevant environmental fungus Alternaria. We also generated bone marrow chimeras to assess whether Cd38(+/+) inflammatory cells would restore AHR in the CD38-deficient (Cd38(-/-)) hosts following ovalbumin challenge. Results show that wild-type (WT) mice develop greater AHR to inhaled methacholine than Cd38(-/-) mice following challenge with either allergen, with comparable airway inflammation. Reciprocal bone marrow transfers did not change the native airway phenotypic differences between WT and Cd38(-/-) mice, indicating that the lower airway reactivity of Cd38(-/-) mice stems from Cd38(-/-) lung parenchymal cells. Following bone marrow transfer from either source and ovalbumin challenge, the phenotype of Cd38(-/-) hosts was partially reversed, whereas the airway phenotype of the WT hosts was preserved. Airway inflammation was similar in Cd38(-/-) and WT chimeras. These results indicate that loss of CD38 on hematopoietic cells is not sufficient to prevent AHR and that the magnitude of airway inflammation is not the predominant underlying determinant of AHR in mice.
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