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Conference Paper: Lipidomics Analysis of Rhinovirus Infection in Human Airway Epithelial Cells

TitleLipidomics Analysis of Rhinovirus Infection in Human Airway Epithelial Cells
Authors
Issue Date2017
PublisherOxford University Press (OUP). The Journal's web site is located at http://ofid.oxfordjournals.org/
Citation
IDWeek 2017, San Diego, CA, 4-8 October 2017. In Open Forum Infectious Diseases, 2017, v. 4 n. Suppl. 1, p. S223 How to Cite?
AbstractBackground: Rhinovirus is one of the most frequently detected respiratory viruses in adult patients with pneumonia or exacerbation of chronic lung diseases. Severe rhinovirus infection is increasingly recognized. High mortality rates have been reported for hospitalized patients. No specific antiviral treatment is currently available. To have a better understanding on the pathogenesis of rhinovirus infection, we analyzed the lipid mediator profile of rhinovirus infection in a human airway epithelial cell line (Calu-3), and compared to those of influenza A virus (IAV)- and influenza B virus (IBV)-infected cells. Lipid mediators were analyzed because these have been shown to regulate host inflammatory response for many types of virus infection, but have not been studied in rhinovirus infection. Methods: Calu-3 was infected with rhinovirus, IAV, or IBV, or mocked infected at 37°C. Cell lysate was collected for targeted lipidomic analysis using ultra-high-performance liquid chromatography-electrospray ionization-quadruple time-of-flight mass spectrometry (UHPLC-ESI-QTOFMS). A bioactive lipid screening library was used as standards. Viral load and cytokine/chemokine RNA expression were also determined. Results: Rhinovirus, IAV and IBV replicated in Calu-3 cells at 37°C. Rhinovirus infection elicited the expression of IL-6, TNF-α, IP-10, IFN-β and IFN-λ1, although at a lower level than that of influenza A or influenza B virus. While the levels of lipid mediators in the n-3 and n-6 polyunsaturated fatty acid (PUFA) pathways were higher in IAV- or IBV-infected cells than mock-infected controls, the levels of most lipid mediators in rhinovirus-infected cells were similar to those found in mock-infected controls. Unexpectedly, the levels of specialized pro-resolving mediators (SPMs) in rhinovirus-infected cells were lower than those of mock-infected controls. Conclusion: There is marked difference in the lipid mediator profile between rhinovirus and influenza virus-infected cells. Since SPMs have been shown to be important for the regulation of inflammation and viral replication for other viruses, such as influenza A virus, the role of SPMs in rhinovirus infection should be further pursued.
DescriptionPoster Abstract Session 69: Immunology - Host Response - no. 606
Persistent Identifierhttp://hdl.handle.net/10722/260773
ISSN
2020 Impact Factor: 3.835
2020 SCImago Journal Rankings: 1.546

 

DC FieldValueLanguage
dc.contributor.authorTo, KKW-
dc.contributor.authorKe, Y-
dc.contributor.authorDissanayake, DMTK-
dc.contributor.authorDing, SY-
dc.contributor.authorYip, CY-
dc.contributor.authorSze, KH-
dc.contributor.authorYuen, KY-
dc.date.accessioned2018-09-14T08:47:10Z-
dc.date.available2018-09-14T08:47:10Z-
dc.date.issued2017-
dc.identifier.citationIDWeek 2017, San Diego, CA, 4-8 October 2017. In Open Forum Infectious Diseases, 2017, v. 4 n. Suppl. 1, p. S223-
dc.identifier.issn2328-8957-
dc.identifier.urihttp://hdl.handle.net/10722/260773-
dc.descriptionPoster Abstract Session 69: Immunology - Host Response - no. 606-
dc.description.abstractBackground: Rhinovirus is one of the most frequently detected respiratory viruses in adult patients with pneumonia or exacerbation of chronic lung diseases. Severe rhinovirus infection is increasingly recognized. High mortality rates have been reported for hospitalized patients. No specific antiviral treatment is currently available. To have a better understanding on the pathogenesis of rhinovirus infection, we analyzed the lipid mediator profile of rhinovirus infection in a human airway epithelial cell line (Calu-3), and compared to those of influenza A virus (IAV)- and influenza B virus (IBV)-infected cells. Lipid mediators were analyzed because these have been shown to regulate host inflammatory response for many types of virus infection, but have not been studied in rhinovirus infection. Methods: Calu-3 was infected with rhinovirus, IAV, or IBV, or mocked infected at 37°C. Cell lysate was collected for targeted lipidomic analysis using ultra-high-performance liquid chromatography-electrospray ionization-quadruple time-of-flight mass spectrometry (UHPLC-ESI-QTOFMS). A bioactive lipid screening library was used as standards. Viral load and cytokine/chemokine RNA expression were also determined. Results: Rhinovirus, IAV and IBV replicated in Calu-3 cells at 37°C. Rhinovirus infection elicited the expression of IL-6, TNF-α, IP-10, IFN-β and IFN-λ1, although at a lower level than that of influenza A or influenza B virus. While the levels of lipid mediators in the n-3 and n-6 polyunsaturated fatty acid (PUFA) pathways were higher in IAV- or IBV-infected cells than mock-infected controls, the levels of most lipid mediators in rhinovirus-infected cells were similar to those found in mock-infected controls. Unexpectedly, the levels of specialized pro-resolving mediators (SPMs) in rhinovirus-infected cells were lower than those of mock-infected controls. Conclusion: There is marked difference in the lipid mediator profile between rhinovirus and influenza virus-infected cells. Since SPMs have been shown to be important for the regulation of inflammation and viral replication for other viruses, such as influenza A virus, the role of SPMs in rhinovirus infection should be further pursued.-
dc.languageeng-
dc.publisherOxford University Press (OUP). The Journal's web site is located at http://ofid.oxfordjournals.org/-
dc.relation.ispartofOpen Forum Infectious Diseases-
dc.relation.ispartofIDWeek-
dc.titleLipidomics Analysis of Rhinovirus Infection in Human Airway Epithelial Cells-
dc.typeConference_Paper-
dc.identifier.emailTo, KKW: kelvinto@hku.hk-
dc.identifier.emailKe, Y: keyh@HKUCC-COM.hku.hk-
dc.identifier.emailYip, CY: yipcyril@hku.hk-
dc.identifier.emailSze, KH: khsze@hku.hk-
dc.identifier.emailYuen, KY: kyyuen@hkucc.hku.hk-
dc.identifier.authorityTo, KKW=rp01384-
dc.identifier.authorityYip, CY=rp01721-
dc.identifier.authoritySze, KH=rp00785-
dc.identifier.authorityYuen, KY=rp00366-
dc.identifier.doi10.1093/ofid/ofx163.462-
dc.identifier.hkuros290975-
dc.identifier.volume4-
dc.identifier.issueSuppl. 1-
dc.identifier.spageS223-
dc.identifier.epageS223-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl2328-8957-

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