Cited by 155Antimicrobial Peptides and ActivitiesRespiratory viral infections researchinterferon and immune responses

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Human Rhinovirus Infection Induces Airway Epithelial Cell Production of Human β-Defensin 2 Both In Vitro and In Vivo

Proud, David, Sanders, Scherer P, Wiehler, Shahina·2004·The Journal of Immunology

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Abstract

We hypothesized that airway epithelial cells, the primary site of human rhinovirus (HRV) infection, provide a link between the innate and specific immune response to HRV via production of human β-defensin (HBD)-2, a potent in vitro attractant and activator of immature dendritic cells. Infection of primary cultures of human epithelial cells with several HRV serotypes induced expression of HBD-2 mRNA and protein, indicating that HBD-2 production was independent of viral receptor usage or mechanisms of viral RNA internalization. Induction of HBD-2 was dependent upon viral replication and could be mimicked by transfection of cells with synthetic dsRNA, but was not dependent upon epithelial production of IL-1. Studies with stable epithelial cell lines expressing HBD-2 promoter constructs, as well as inhibitor studies in primary cells, both demonstrated that induction of HBD-2 involves activation of the transcription factor, NF-κB. Other transcription factors must also be activated by HRV infection, however, as expression of HBD-3 mRNA was also induced and there is no putative NF-κB recognition sequence in the promoter of this gene. HBD-2 showed no direct antiviral activity against HRV. In vivo infection of normal human subjects with HRV-16 induced expression of mRNA for HBD-2 in nasal epithelial scrapings. Increases in mRNA correlated with viral titer and with increased levels of HBD-2 protein in nasal lavages. This represents the first demonstration that HRV infection induces epithelial expression of HBD-2 both in vitro and in vivo, and supports the concept that HBD-2 may play a role in host defense to HRV infection.

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Authors: Proud, D., Sanders, S. P., & Wiehler, S.
Affiliations: University of Calgary (CA)
Johns Hopkins University (US)
ORCID: Proud, David
Wiehler, Shahina
Venue: The Journal of Immunology
Publisher: Oxford University Press (OUP)
Published: 2004-04-01
Volume: 172
Issue: 7
Pages: 4637-4645
ISSN: 0022-1767 (ISSN-L)
1550-6606
DOI: 10.4049/jimmunol.172.7.4637
OpenAlex: W2115289014
Cited by: 154
References: 64
Citations by year: 2025: 5 · 2024: 2 · 2023: 1 · 2022: 1 · 2021: 5 · 2020: 6 · 2019: 4 · 2018: 10 · 2017: 5 · 2016: 9 · 2015: 10 · 2014: 4 · 2013: 6 · 2012: 7
FWCI: 8.54
Type: journal article
Language: en
Open access: closed
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations: The Journal of Immunology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r01hl061011-02)
National Heart, Lung, and Blood Institute (HL 61011)
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 › interferon and immune responses
Keywords: human rhinovirus, human beta-defensin 2, airway epithelial cells, innate immunity, NF-κB, human beta-defensin 3, viral replication, double-stranded RNA, nasal epithelium, host defense, dendritic cell activation
MeSH terms: Adult, Common Cold, Female, Humans, Interleukin-1, Male, Promoter Regions, Genetic, Rhinovirus, RNA, Messenger, RNA, Viral, Serotyping, Time Factors, Virus Replication, NF-kappa B, Respiratory Mucosa, beta-Defensins, Virus Inactivation, Cell Line, Tumor

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Human Rhinovirus Infection Induces Airway Epithelial Cell Production of Human β-Defensin 2 Both In Vitro and In Vivo

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