ArticleRespiratory research2006
Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection.
Article in Respiratory research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 81 citations in OpenAlex.
- Glucocorticoid Insensitivity: Is It a Question of Time and Place?Biomedicines · 2025Review
- Rhinovirus C15 Attenuates Relaxation and cAMP Production in Human Airways and Smooth Muscle.American journal of respiratory cell and molecular biology · 2023Article
- Insights into glucocorticoid responses derived from omics studies.Pharmacology & therapeutics · 2021Review
- Viral Induced Effects on a Vulnerable Epithelium; Lessons Learned From Paediatric Asthma and Eosinophilic Oesophagitis.Frontiers in immunology · 2021Review
- Metal-Stimulated Interleukin-6 Production Through a Proton-Sensing Receptor, Ovarian Cancer G Protein-Coupled Receptor 1, in Human Bronchial Smooth Muscle Cells: A Response Inhibited by Dexamethasone.Journal of inflammation research · 2021Article
- Effects of ATP-competitive and function-selective ERK inhibitors on airway smooth muscle cell proliferation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Article
- Extracellular acidification-induced CXCL8 production through a proton-sensing receptor OGR1 in human airway smooth muscle cells: a response inhibited by dexamethasone.Journal of inflammation (London, England) · 2019Article
- Phenotype and Functional Features of Human Telomerase Reverse Transcriptase Immortalized Human Airway Smooth Muscle Cells from Asthmatic and Non-Asthmatic Donors.Scientific reports · 2018Article
- A novel immunomodulatory function of neutrophils on rhinovirus-activated monocytes in vitro.Thorax · 2016Article
- Biomass Smoke Exposure Enhances Rhinovirus-Induced Inflammation in Primary Lung Fibroblasts.International journal of molecular sciences · 2016Article
- The role of viral infections in exacerbations of chronic obstructive pulmonary disease and asthma.Therapeutic advances in respiratory disease · 2016Review
- TLR3 activation increases chemokine expression in human fetal airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Glucocorticoid genes and the developmental origins of asthma susceptibility and treatment response.American journal of respiratory cell and molecular biology · 2015Article
- Altered Innate Immune Responses in Neutrophils from Patients with Well- and Suboptimally Controlled Asthma.Mediators of inflammation · 2015Article
- The Three A's in Asthma - Airway Smooth Muscle, Airway Remodeling & Angiogenesis.The open respiratory medicine journal · 2015Article
- Inhibition of phosphodiesterase 4 modulates cytokine induction from toll like receptor activated, but not rhinovirus infected, primary human airway smooth muscle.Respiratory research · 2013Article
- Article
- Rhinovirus and dsRNA induce RIG-I-like receptors and expression of interferon β and λ1 in human bronchial smooth muscle cells.PloS one · 2013Article
- Virus infection-induced bronchial asthma exacerbation.Pulmonary medicine · 2012Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExacerbations of asthma are associated with viral respiratory tract infections, of which rhinoviruses (RV) are the predominant virus type. Airway smooth muscle is important in asthma pathogenesis, however little is known about the potential interaction of RV and human airway smooth muscle cells (HASM). We hypothesised that rhinovirus induction of inflammatory cytokine release from airway smooth muscle is augmented and differentially regulated in asthmatic compared to normal HASM cells.
methodsHASM cells, isolated from either asthmatic or non-asthmatic subjects, were infected with rhinovirus. Cytokine production was assayed by ELISA, ICAM-1 cell surface expression was assessed by FACS, and the transcription regulation of IL-6 was measured by luciferase activity.
resultsRV-induced IL-6 release was significantly greater in HASM cells derived from asthmatic subjects compared to non-asthmatic subjects. This response was RV specific, as 5% serum- induced IL-6 release was not different in the two cell types. Whilst serum stimulated IL-8 production in cells from both subject groups, RV induced IL-8 production in only asthmatic derived HASM cells. The transcriptional induction of IL-6 was differentially regulated via C/EBP in the asthmatic and NF-kappaB + AP-1 in the non-asthmatic HASM cells.
conclusionThis study demonstrates augmentation and differential transcriptional regulation of RV specific innate immune response in HASM cells derived from asthmatic and non-asthmatics, and may give valuable insight into the mechanisms of RV-induced asthma exacerbations.
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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.