ArticleBritish journal of pharmacology1999
Induction of eotaxin expression and release from human airway smooth muscle cells by IL-1beta and TNFalpha: effects of IL-10 and corticosteroids.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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
25 citing papers in PubMed, 96 citations in OpenAlex.
- Kiss1 receptor knockout exacerbates airway hyperresponsiveness and remodeling in a mouse model of allergic asthma.Respiratory research · 2024Article
- Glucocorticoid Insensitivity in Asthma: The Unique Role for Airway Smooth Muscle Cells.International journal of molecular sciences · 2022Review
- Important lessons learned from studies on the pharmacology of glucocorticoids in human airway smooth muscle cells: Too much of a good thing may be a problem.Pharmacology & therapeutics · 2020Review
- CCL11 (Eotaxin-1) Levels Predict Long-Term Functional Outcomes in Patients Following Ischemic Stroke.Translational stroke research · 2017Article
- Regulation of human airway smooth muscle cell migration and relevance to asthma.Respiratory research · 2017Review
- Focal adhesion kinase (FAK) and mechanical stimulation negatively regulate the transition of airway smooth muscle tissues to a synthetic phenotype.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Effects of copy center particles on the lungs: a toxicological characterization using a Balb/c mouse model.Inhalation toxicology · 2013Article
- Airway smooth muscle in the pathophysiology and treatment of asthma.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Review
- Tenascin-C deficiency in apo E-/- mouse increases eotaxin levels: implications for atherosclerosis.Atherosclerosis · 2013Article
- Inflammation signals airway smooth muscle cell proliferation in asthma pathogenesis.Multidisciplinary respiratory medicine · 2013Article
- Corticosteroid insensitivity of chemokine expression in airway smooth muscle of patients with severe asthma.The Journal of allergy and clinical immunology · 2012Article
- Airway smooth muscle in asthma: just a target for bronchodilation?Clinics in chest medicine · 2012Review
- MAPK regulation of IL-4/IL-13 receptors contributes to the synergistic increase in CCL11/eotaxin-1 in response to TGF-β1 and IL-13 in human airway fibroblasts.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- PPARγ Ligands Regulate Noncontractile and Contractile Functions of Airway Smooth Muscle: Implications for Asthma Therapy.PPAR research · 2012Article
- Distribution of major basic protein on human airway following in vitro eosinophil incubation.Mediators of inflammation · 2010Article
- Mechanistic systems biology of inflammatory gene expression in airway smooth muscle as tool for asthma drug development.Current drug discovery technologies · 2008Review
- Role of IL-10 in the resolution of airway inflammation.Current molecular medicine · 2008Review
- Cytokine expression in CD4(+) cells exposed to the monocyte locomotion inhibitory factor produced by Entamoeba histolytica.Parasitology research · 2006Article
- Cigarette smoke induces IL-8, but inhibits eotaxin and RANTES release from airway smooth muscle.Respiratory research · 2005Article
- IL-10 and its related cytokines for treatment of inflammatory bowel disease.World journal of gastroenterology · 2004Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Eotaxin is a novel C-C chemokine with selective chemoattractant activity for eosinophils. We determined whether eotaxin could be produced by human airway smooth muscle (HASM) cells in culture and examined its regulation by interleukin-10 (IL-10) and the corticosteroid, dexamethasone. Stimulation of the cells with interleukin-1beta (IL-1beta) or tumour necrosis factor (TNFalpha) each at 10 ng ml(-1) induced the release of eotaxin protein with maximal accumulation by 24 h. Interferon-gamma (IFNgamma) alone at 10 ng ml(-1) had no effect and there was no synergy between these cytokines on the release of eotaxin. Reverse phase high performance liquid chromatographic (HPLC) analysis of supernatents from cells treated with TNFalpha (10 ng ml(-1) for 96 h showed immunoreactivity to eotaxin which eluted with the expected retention time of 34.5-35 min. Both IL-1beta and TNFalpha-induced release of eotaxin was not inhibited by dexamethasone (1 microM), however IL-10 (10 ng ml(-1)) had a significant inhibitory effect. Dexamethasone and IL-10 did not inhibit the induction of eotaxin mRNA induced by IL-1beta or TNFalpha. Thus, human airway smooth muscle cells can release eotaxin and could be an important source of chemokine production during airway inflammatory events.
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