ArticleThe Journal of clinical investigation1999
Regulation of TH1- and TH2-type cytokine expression and action in atopic asthmatic sensitized airway smooth muscle.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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.
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Who cites it
30 citing papers in PubMed, 131 citations in OpenAlex.
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- The proprotein convertase furin inhibits IL-13-induced inflammation in airway smooth muscle by regulating integrin-associated signaling complexes.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Allergic Inflammation Caused by Dimerized Translationally Controlled Tumor Protein is Attenuated by Cardamonin.Frontiers in pharmacology · 2021Article
- Targeting IL-5 pathway against airway hyperresponsiveness: A comparison between benralizumab and mepolizumab.British journal of pharmacology · 2020Article
- Review
- Differential regulation of cytokine and chemokine expression by MK2 and MK3 in airway smooth muscle cells.Pulmonary pharmacology & therapeutics · 2018Article
- Smooth muscle CaMKIIδ promotes allergen-induced airway hyperresponsiveness and inflammation.Pflugers Archiv : European journal of physiology · 2015Article
- CCL2 release by airway smooth muscle is increased in asthma and promotes fibrocyte migration.Allergy · 2014Article
- Changes in the expression of smooth muscle contractile proteins in TNBS- and DSS-induced colitis in mice.Inflammation · 2013Article
- CaMKII is essential for the proasthmatic effects of oxidation.Science translational medicine · 2013Article
- Eosinophils induce airway smooth muscle cell proliferation.Journal of clinical immunology · 2013Article
- Airway smooth muscle in asthma: just a target for bronchodilation?Clinics in chest medicine · 2012Review
- T-bet is induced by interferon-γ to mediate chemokine secretion and migration in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- The pivotal role of airway smooth muscle in asthma pathophysiology.Journal of allergy · 2011Article
- Novel method of monitoring trace cytokines and activated STAT molecules in the paws of arthritic mice using multiplex bead technology.BMC immunology · 2010Article
- Bronchial epithelial cells produce IL-5: implications for local immune responses in the airways.Cellular immunology · 2010Article
- Current status and challenges of cytokine pharmacology.British journal of pharmacology · 2009Review
- RNA interference against interleukin-5 attenuates airway inflammation and hyperresponsiveness in an asthma model.Journal of Zhejiang University. Science. B · 2009Article
- Research upregulation of CD23 (FcepsilonRII) expression in human airway smooth muscle cells (huASMC) in response to IL-4, GM-CSF, and IL-4/GM-CSF.Clinical and molecular allergy : CMA · 2005Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
CD4(+) T helper (TH)1- and TH2-type cytokines reportedly play an important role in the pathobiology of asthma. Recent evidence suggests that proasthmatic changes in airway smooth muscle (ASM) responsiveness may be induced by the autocrine release of certain proinflammatory cytokines by the ASM itself. We examined whether TH1- and TH2-type cytokines are expressed by atopic asthmatic sensitized ASM and serve to autologously regulate the proasthmatic phenotype in the sensitized ASM. Expression of these cytokines and their receptors was examined in isolated rabbit and human ASM tissues and cultured cells passively sensitized with sera from atopic asthmatic patients or control subjects. Relative to controls, atopic sensitized ASM cells exhibited an early increased mRNA expression of the TH2-type cytokines, interleukin-5 (IL-5) and granulocyte-macrophage colony-stimulating factor (GM-CSF), and their receptors. This was later followed by enhanced mRNA expression of the TH1-type cytokines, IL-2, IL-12, and interferon-gamma (IFN-gamma), as well as their respective receptors. In experiments on isolated ASM tissue segments (a) exogenous administration of IL-2 and IFN-gamma to atopic asthmatic serum-sensitized ASM ablated both their enhanced constrictor responsiveness to acetylcholine (ACh) and their attenuated relaxation responsiveness to beta-adrenoceptor stimulation with isoproterenol, and (b) administration of IL-5 and GM-CSF to naive ASM induced significant increases in their contractility to ACh and impaired their relaxant responsiveness to isoproterenol. Collectively, these observations provide new evidence demonstrating that human ASM endogenously expresses both TH1- and TH2-type cytokines and their receptors, that these molecules are sequentially upregulated in the atopic asthmatic sensitized state, and that they act to downregulate and upregulate proasthmatic perturbations in ASM responsiveness, respectively.
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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.