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Cited by 23Asthma and respiratory diseasesRespiratory viral infections researchNeonatal Respiratory Health Research

Respiratory syncytial virus augments production of fibroblast growth factor basic in vitro: Implications for a possible mechanism of prolonged wheezing after infection

Dosanjh, A., Rednam, S., Martin, M.·2003·Pediatric Allergy and Immunology
DOI 10.1046/j.0905-6157.2003.00090.x
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Abstract

Respiratory syncytial virus (RSV) has been linked to the development of clinical asthma. Cellular mechanisms of this observation are not yet clearly elucidated. In chronic asthma, production of growth factors and remodeling are associated with prolonged wheezing. It was hypothesized that cells infected with RSV may produce excessive levels of fibroblast growth factor basic (FGFb), and epidermal growth factor (EGF). Airway epithelial cells were incubated with either: (i) virus, (ii) inactivated virus, or (iii) media only. The levels of FGFb and EGF were measured in the cellular supernatant fluid. The study demonstrated that by 24 h after RSV inoculation, or exposure to RSV‐killed virus, cells are stimulated to produce significantly more FGFb, compared with non‐infected/non‐exposed control cells. FGFb is an important factor in remodeling and fibroblast activation in the airway. Using treatment with actinomycin D and cylcohexamide the effect of inhibiting translation or transcription in the infected cells, on FGFb production was demonstrated. There were no alterations in EGF production detectable. Based on the findings, the mechanism of FGFb secretion after RSV inoculation, appears to be regulated at the levels of both transcription and translation. The increased FGFb release potentially could contribute to fibroblast activation and remodeling in the airway, and thus provide another possible mechanism for prolonged wheezing after infection.

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  • β2 agonists have been shown to reduce bacterium- and toxin-induced epithelial cell damage in models of nasal epithelial culture.

    “β2 agonists have been shown to reduce bacterium- and toxin-induced epithelial cell damage in models of nasal epithelial culture (53, 54).”

    From The airway epithelium: soldier in the fight against respiratory viruses (2011) · cites this paper as [54]

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Authors
Dosanjh, A., Rednam, S., & Martin, M.
Affiliations
St. Jude Children's Research Hospital (US)
Corresponding author
Dosanjh, A.
ORCID
Dosanjh, A.
Venue
Pediatric Allergy and Immunology
Publisher
Wiley
Published
2003-12
Volume
14
Issue
6
Pages
437-440
ISSN
  • 0905-6157 (ISSN-L)
  • 1399-3038
DOI
10.1046/j.0905-6157.2003.00090.x
OpenAlex
W2077236378
Cited by
23
References
20
Citations by year
2021: 1 · 2020: 2 · 2019: 1 · 2015: 1 · 2014: 1 · 2012: 2
FWCI
1.53
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 10 d)
Locations
  • Pediatric Allergy and Immunology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
  • Health Sciences › Medicine › Epidemiology › Respiratory viral infections research
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Neonatal Respiratory Health Research
Keywords
respiratory syncytial virus, epidermal growth factor, airway epithelial cells, airway remodeling, fibroblast activation, asthma, viral infection, transcriptional regulation, translational regulation, actinomycin D, cycloheximide
MeSH terms
Bronchi, Cell Survival, Dactinomycin, Epidermal Growth Factor, Epithelial Cells, Fibroblast Growth Factors, Humans, Protein Synthesis Inhibitors, Respiratory Sounds, Respiratory Syncytial Viruses, Virus Replication, Respiratory Syncytial Virus Infections, Virus Inactivation

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