Synergistic effects of fluticasone propionate and salmeterol on inhibiting rhinovirus‐induced epithelial production of remodelling‐associated growth factors
Abstract
Summary: Background Rhinoviruses (RV), the major trigger of acute asthma exacerbations, are able to infect bronchial epithelium and induce production of pro‐inflammatory, but also angiogenic and pro‐fibrotic mediators. Fluticasone propionate (FP) and salmeterol (S) are clinically effective and act synergistically in controlling persistent asthma; however, their effect on virus‐associated asthma is less clear. Aim The aim of this study was to assess the individual and combined effects of FP and S on RV‐induced epithelial production of vascular endothelial growth factor (VEGF) and fibroblast growth factor‐2 (FGF‐2). Methods Bronchial epithelial cells (BEAS‐2B) were exposed in vitro to RV and were subsequently treated with FP and S, at physiologically relevant concentrations, alone or in combination. VEGF and FGF‐2 were measured in the supernatants of these cultures using ELISA. Results FP was able to reduce RV‐induced VEGF production in a dose‐dependent manner. S also induced a smaller reduction; addition of both factors inhibited VEGF synergistically. FGF‐2 production was not inhibited by either FP or S alone, but was significantly reduced when both substances were present in the culture. Conclusion This study demonstrates that FP and S may synergistically inhibit the production of angiogenic and/or pro‐fibrotic factors that are induced after RV infection of BEAS‐2B and are implicated in airway remodelling, suggesting that this combination may represent an important therapeutic option on virus‐induced asthma.
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Approximately 90% of inhaled particles, including respiratory viruses, are transported with mucus from the bronchioles to the trachea by the beats of cilia present on the surfaces of airway epithelial cells.
“Approximately 90% of inhaled particles, including respiratory viruses, are transported with mucus from the bronchioles to the trachea by the beats of cilia present on the surfaces of airway epithelial cells (299).”
From The airway epithelium: soldier in the fight against respiratory viruses (2011) · cites this paper as [299]
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The airway epithelium: soldier in the fight against respiratory viruses
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Self-citation
- Authors
- Volonaki, E., Psarras, S., Xepapadaki, P., Psomali, D., Gourgiotis, D., & Papadopoulos, N. G.
- Affiliations
- National and Kapodistrian University of Athens (GR)
- Corresponding author
- Papadopoulos, N. G.
- Venue
- Clinical & Experimental Allergy
- Publisher
- Wiley
- Published
- 2006-10
- Volume
- 36
- Issue
- 10
- Pages
- 1268-1273
- ISSN
- 0954-7894 (ISSN-L)
- 1365-2222
- OpenAlex
- W1986254137
- Cited by
- 44
- References
- 38
- Citations by year
- 2026: 1 · 2025: 2 · 2023: 3 · 2022: 3 · 2021: 1 · 2019: 1 · 2017: 1 · 2016: 2 · 2015: 2 · 2013: 3 · 2012: 3
- FWCI
- 3.51
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical & Experimental Allergy (publishedVersion)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Occupational exposure and asthma
- Keywords
- fluticasone propionate, salmeterol, rhinovirus, airway remodeling, vascular endothelial growth factor, fibroblast growth factor 2, bronchial epithelial cells, BEAS-2B, drug synergy, anti-inflammatory therapy, angiogenesis, airway fibrosis
- MeSH terms
- Fluticasone, Salmeterol Xinafoate, Albuterol, Androstadienes, Anti-Inflammatory Agents, Bronchi, Cell Line, Dose-Response Relationship, Drug, Drug Synergism, Enzyme-Linked Immunosorbent Assay, Epithelial Cells, HeLa Cells, Humans, Picornaviridae Infections, Rhinovirus, Fibroblast Growth Factor 2, Intercellular Signaling Peptides and Proteins, Vascular Endothelial Growth Factor A
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