Cited by 135Antimicrobial Peptides and ActivitiesRespiratory viral infections researchImmune Response and Inflammation

Rhinovirus increases human β-defensin-2 and -3 mRNA expression in cultured bronchial epithelial cells

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Duits, Louise A, Nibbering, Peter H, Strijen, Elisabeth, Vos, Joost B, Mannesse-Lazeroms, Sylvia P.G, Sterkenburg, Marianne A.J.A, Hiemstra, Pieter S·2003·FEMS Immunology & Medical Microbiology

Abstract

Human beta-defensins (hBDs) are antimicrobial peptides that play important roles in host defense against infection, inflammation and immunity. Previous studies showed that micro-organisms and proinflammatory mediators regulate the expression of these peptides in airway epithelial cells. The aim of the present study was to investigate the modulation of expression of hBDs in cultured primary bronchial epithelial cells (PBEC) by rhinovirus-16 (RV16), a respiratory virus responsible for the common cold and associated with asthma exacerbations. RV16 was found to induce expression of hBD-2 and -3 mRNA in PBEC, but did not affect hBD-1 mRNA. Viral replication appeared essential for rhinovirus-induced beta-defensin mRNA expression, since UV-inactivated rhinovirus did not increase expression of hBD-2 and hBD-3 mRNA. Exposure to synthetic double-stranded RNA (dsRNA) molecule polyinosinic:polycytidylic acid had a similar effect as RV16 on mRNA expression of these peptides in PBEC. In line with this, PBEC were found to express TLR3, a Toll-like receptor involved in recognition of dsRNA. This study shows that rhinovirus infection of PBEC leads to increased hBD-2 and hBD-3 mRNA expression, which may play a role in both the uncomplicated common cold and in virus-associated exacerbations of asthma.

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  • Similar associations between inflammatory mediators and disease severity have been demonstrated in the context of influenza virus, coronavirus, and parainfluenza virus infections.

    “Similar associations have been demonstrated in the context of influenza virus (21, 43, 206, 283), coronavirus (328), and parainfluenza virus (58) infections.”

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  1. Rueckert, R.R. (1996) Picornaviridae and their replication. Fields Virology (Fields, B.N., Knipe, D.M., Howley, P.M., Chanock, R.M., Melnick, J.L., Monath, T.P., Roizman, B. and Strauss, S.E., Eds.), pp. 609^654. Lippencott-Raven Publishers, Philadelphia.

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Authors
Duits, L. A., Nibbering, P. H., Strijen, E., Vos, J. B., Mannesse-Lazeroms, S. P. G., Sterkenburg, M. A. J. A., & Hiemstra, P. S.
Affiliations
Leiden University Medical Center (NL)
Corresponding author
Hiemstra, Pieter S
Venue
FEMS Immunology & Medical Microbiology
Published
2003-08
Volume
38
Issue
1
Pages
59-64
ISSN
  • 0928-8244 (ISSN-L)
  • 1574-695X
OpenAlex
W2076513631
Cited by
135
References
46
Citations by year
2026: 2 · 2025: 4 · 2024: 1 · 2023: 3 · 2022: 4 · 2021: 5 · 2020: 5 · 2019: 4 · 2018: 6 · 2017: 6 · 2016: 9 · 2015: 5 · 2014: 8 · 2013: 2 · 2012: 5
FWCI
8.13
Type
journal article
Language
en
Open access
Locations
  • FEMS Immunology & Medical Microbiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Nederlandse Organisatie voor Wetenschappelijk Onderzoek
Topics
  • Life Sciences › Immunology and Microbiology › Microbiology › Antimicrobial Peptides and Activities
  • Health Sciences › Medicine › Epidemiology › Respiratory viral infections research
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
rhinovirus 16, human beta-defensin 2, human beta-defensin 3, beta-defensin 1, bronchial epithelial cells, antimicrobial peptides, viral infection, viral replication, double-stranded RNA, poly(I:C), TLR3, common cold, asthma exacerbations, airway epithelium
MeSH terms
Bronchi, Cells, Cultured, Epithelial Cells, Gene Expression Regulation, Humans, Rhinovirus, RNA, Messenger, Gene Expression, beta-Defensins

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