ArticleJournal of inflammation (London, England)2015
Human parainfluenza virus type 3 (HPIV3) induces production of IFNγ and RANTES in human nasal epithelial cells (HNECs).
Article in Journal of inflammation (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Differential Induction and Signaling of Type I and III Interferons During Infection of Human Nasal Epithelial Cells With the Four Human Parainfluenza Virus Types.Journal of medical virology · 2026Article
- The role of virus in nasal inflammation.European journal of medical research · 2025Review
- The Role of Gut Microbiota in the Modulation of Pulmonary Immune Response to Viral Infection Through the Gut-Lung Axis.Journal of inflammation research · 2025Review
- A robust mouse model of HPIV-3 infection and efficacy of GS-441524 against virus-induced lung pathology.Nature communications · 2024Article
- SARS-CoV-2 and Other Respiratory Viruses in Human Olfactory Pathophysiology.Microorganisms · 2024Review
- Bioengineered Co-culture of organoids to recapitulate host-microbe interactions.Materials today. Bio · 2022Review
- Polarization of protease-activated receptor 2 (PAR-2) signaling is altered during airway epithelial remodeling and deciliation.The Journal of biological chemistry · 2020Article
- Toll-Like Receptor Agonists Modulate Wound Regeneration in Airway Epithelial Cells.International journal of molecular sciences · 2018Article
- A pilot study on primary cultures of human respiratory tract epithelial cells to predict patients' responses to H7N9 infection.Oncotarget · 2018Article
- Inflammasome Antagonism by Human Parainfluenza Virus Type 3 C Protein.Journal of virology · 2018Article
- MERS-CoV and H5N1 influenza virus antagonize antigen presentation by altering the epigenetic landscape.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- UK circulating strains of human parainfluenza 3: an amplicon based next generation sequencing method and phylogenetic analysis.Wellcome open research · 2018Article
- Characterizing the Cellular Immune Response to Parainfluenza Virus 3.The Journal of infectious diseases · 2017Article
- The Role of Human Parainfluenza Virus Infections in the Immunopathology of the Respiratory Tract.Current allergy and asthma reports · 2017Review
- Impaired virus replication and decreased innate immune responses to viral infections in nasal epithelial cells from patients with allergic rhinitis.Clinical and experimental immunology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHuman parainfluenza virus type 3 (HPIV3), while infecting lower airway epithelial cells induces pneumonia and bronchiolitis in infants and children, and may lead to asthma exacerbations in children and adults. Respiratory viruses invading the airway epithelium activate innate immune response and induce inflammatory cytokine release contributing to the pathophysiology of upper and lower airway disorders. However, the effects of HPIV3 infection on nasal epithelial cells have not been well defined. The aim of this study was to evaluate the effect of the HPIV3 infection on cultured human nasal epithelial cells (HNECs) and the release of interferon gamma and other cytokines.
methodsRPMI 2650, a human nasal epithelial cell line was cultured into confluence and was infected with HPIV3 (MOI of 0.1, 0.01 and 0.001). The protein release into supernatants and mRNA expression of selected cytokines were assessed 24, 48 and 72 h after infection. Cytokine concentrations in supernatants were measured by ELISA and expression of cytokine mRNA in RPMI 2650 cells confirmed by real time RT-PCR analysis.
resultsHNECs infection with HPIV3 did not induce cytotoxicity for at least 48 hours, but significantly increased IFN-γ protein concentration in the cell supernatants at 24 h and 48 h post infection (by 387% and 485% respectively as compared to mock infected cells). At 24 h a significant increase in expression of mRNA for IFNγ was observed. RANTES protein concentration and mRNA expression were significantly increased at 72 h after infection (mean protein concentration: 3.5 ± 1.4 pg/mL for 0.001 MOI, 10.8 ± 4.6 pg/mL for 0.01 MOI and 61.5 ± 18.4 pg/mL for 0.1 MOI as compared to 2.4 ± 1.3 pg/mL for uninfected cells). No measurable concentrations of TNF-α, IL-10, TSLP, IL-8, GM-CSF or eotaxin, were detected in virus infected cells supernatants.
conclusionsHPIV3 effectively infects upper airway epithelial cells and the infection is associated with induction of IFN-γ and generation of RANTES.
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