ArticleImmunobiology2008
Essential role of IFNbeta and CD38 in TNFalpha-induced airway smooth muscle hyper-responsiveness.
Article in Immunobiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- The Impact of Corticosteroids on Human Airway Smooth Muscle Contractility and Airway Hyperresponsiveness: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Insights on inflammatory pathways and their cross-talk: a comprehensive review on asthma.Molecular biology reports · 2025Review
- Role of CD38/cADPR signaling in obstructive pulmonary diseases.Current opinion in pharmacology · 2020Review
- Kininogen deficiency or depletion reduces enhanced pause independent of pulmonary inflammation in a house dust mite-induced murine asthma model.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- CD38/cADPR Signaling Pathway in Airway Disease: Regulatory Mechanisms.Mediators of inflammation · 2018Review
- TNFα enhances force generation in airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- CD38 in the pathogenesis of allergic airway disease: Potential therapeutic targets.Pharmacology & therapeutics · 2017Review
- Group 2 innate lymphoid cells mediate ozone-induced airway inflammation and hyperresponsiveness in mice.The Journal of allergy and clinical immunology · 2016Article
- Dissociation of FK506-binding protein 12.6 kD from ryanodine receptor in bronchial smooth muscle cells in airway hyperresponsiveness in asthma.American journal of respiratory cell and molecular biology · 2014Article
- Airway smooth muscle in airway reactivity and remodeling: what have we learned?American journal of physiology. Lung cellular and molecular physiology · 2013Review
- Smooth muscle hypercontractility in airway hyperresponsiveness: innate, acquired, or nonexistent?Journal of allergy · 2013Article
- The effect of lipoprotein-associated phospholipase A2 deficiency on pulmonary allergic responses in Aspergillus fumigatus sensitized mice.Respiratory research · 2012Article
- The B-cell superantigen Finegoldia magna protein L causes pulmonary inflammation by a mechanism dependent on MyD88 but not B cells or immunoglobulins.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012Article
- Targeting airway smooth muscle in airways diseases: an old concept with new twists.Expert review of respiratory medicine · 2011Review
- Expression and activation of the oxytocin receptor in airway smooth muscle cells: Regulation by TNFalpha and IL-13.Respiratory research · 2010Article
- TLR4 is necessary for hyaluronan-mediated airway hyperresponsiveness after ozone inhalation.American journal of respiratory and critical care medicine · 2010Article
- Transcriptional regulation of cytokine function in airway smooth muscle cells.Pulmonary pharmacology & therapeutics · 2009Review
- Absence of alpha 4 but not beta 2 integrins restrains development of chronic allergic asthma using mouse genetic models.Experimental hematology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
We recently identified autocrine interferon (IFN)beta as a novel mechanism mediating tumor necrosis factor (TNF)alpha-induced expression of inflammatory genes in airway smooth muscle (ASM) cells, including CD38, known to regulate calcium signaling. Here, we investigated the putative involvement of IFNbeta in regulating TNFalpha-induced airway hyper-responsiveness (AHR), a defining feature of asthma. Using our pharmacodynamic model to assess ex vivo AHR isolated murine tracheal rings, we found that TNFalpha-induced enhanced contractile responses to carbachol and bradykinin was abrogated by neutralizing anti-IFNbeta antibody or in tracheal rings deficient in CD38. In cultured human ASM cells, where CD38 has been involved in TNFalpha-induced enhanced calcium signals to carbachol and bradykinin, we found that neutralizing anti-IFNbeta prevented TNFalpha enhancing action only on carbachol responses but not to that induced by bradykinin. In a well-characterized model of allergic asthma (mice sensitized and challenged with Aspergillus fumigatus (Af)), we found heightened expression of both IFNbeta and CD38 in the airways. Furthermore, allergen-associated AHR to methacholine, assessed by lung resistance and dynamic compliance, was completely suppressed in CD38-deficient mice, despite the preservation of airway inflammation. These data provide the first evidence that ASM-derived IFNbeta and CD38 may play a significant role in the development of TNFalpha-associated AHR.
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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.