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Conference Paper: Investigating the role of interleukin-17A on cytokines production by macrophages in response to bacterial infections

TitleInvestigating the role of interleukin-17A on cytokines production by macrophages in response to bacterial infections
Authors
Issue Date2014
PublisherMedcom Limited. The Journal's web site is located at http://www.hkjpaed.org/index.asp
Citation
The 2014 Joint Annual Scientific Meeting of the Hong Kong Paediatric Society and Hong Kong Paediatric Nurses Association, Hong Kong, China, 15 June 2014. In the Hong Kong Journal of Paediatrics (New series), 2014, v. 19 n. 3, p. 202-203 How to Cite?
AbstractInterleukin-17A (IL-17A) has been shown to associate with a variety of infection diseases. In this study, we investigate whether IL-17A affects cytokines production of human peripheral blood-derived macrophages during Mycobacteriun bovis BCG or Klebsiella pneumoniae infection. We observed that IL-17A-treated macrophages exhibited suppressed productions of TNF-α and IL-6 in response to BCG infection. The reduction of cytokines production was not associated with cell death. On the other hand, IL-17A promoted TNF-α and IL-6 production by macrophages during K. pneumoniae infection. Furthermore, IL-17A did not affect TNF-α production induced by LPS and Pam3 Cys, which are TLR4 and TLR2 agonists, respectively. The data suggest that the differential regulation of cytokines production by IL-17A requires whole bacterium infection.
DescriptionPoster Presentation
Persistent Identifierhttp://hdl.handle.net/10722/206051
ISSN
2021 Impact Factor: 0.104
2020 SCImago Journal Rankings: 0.115

 

DC FieldValueLanguage
dc.contributor.authorLing, WLen_US
dc.contributor.authorWang, Len_US
dc.contributor.authorPong, CHen_US
dc.contributor.authorChan, GCFen_US
dc.contributor.authorLi, CBen_US
dc.date.accessioned2014-10-20T11:47:23Z-
dc.date.available2014-10-20T11:47:23Z-
dc.date.issued2014en_US
dc.identifier.citationThe 2014 Joint Annual Scientific Meeting of the Hong Kong Paediatric Society and Hong Kong Paediatric Nurses Association, Hong Kong, China, 15 June 2014. In the Hong Kong Journal of Paediatrics (New series), 2014, v. 19 n. 3, p. 202-203en_US
dc.identifier.issn1013-9923-
dc.identifier.urihttp://hdl.handle.net/10722/206051-
dc.descriptionPoster Presentation-
dc.description.abstractInterleukin-17A (IL-17A) has been shown to associate with a variety of infection diseases. In this study, we investigate whether IL-17A affects cytokines production of human peripheral blood-derived macrophages during Mycobacteriun bovis BCG or Klebsiella pneumoniae infection. We observed that IL-17A-treated macrophages exhibited suppressed productions of TNF-α and IL-6 in response to BCG infection. The reduction of cytokines production was not associated with cell death. On the other hand, IL-17A promoted TNF-α and IL-6 production by macrophages during K. pneumoniae infection. Furthermore, IL-17A did not affect TNF-α production induced by LPS and Pam3 Cys, which are TLR4 and TLR2 agonists, respectively. The data suggest that the differential regulation of cytokines production by IL-17A requires whole bacterium infection.-
dc.languageengen_US
dc.publisherMedcom Limited. The Journal's web site is located at http://www.hkjpaed.org/index.asp-
dc.relation.ispartofHong Kong Journal of Paediatrics (New series)en_US
dc.titleInvestigating the role of interleukin-17A on cytokines production by macrophages in response to bacterial infectionsen_US
dc.typeConference_Paperen_US
dc.identifier.emailLing, WL: lingwl@graduate.hku.hken_US
dc.identifier.emailWang, L: vickyw@hku.hken_US
dc.identifier.emailPong, CH: jchpong@hku.hken_US
dc.identifier.emailChan, GCF: gcfchan@hku.hken_US
dc.identifier.emailLi, CB: jamesli@graduate.hku.hken_US
dc.identifier.authorityChan, GCF=rp00431en_US
dc.identifier.authorityLi, CB=rp00496en_US
dc.description.naturepublished_or_final_version-
dc.identifier.hkuros241331en_US
dc.identifier.volume19-
dc.identifier.issue3-
dc.identifier.spage202-
dc.identifier.epage203-
dc.publisher.placeHong Kong-
dc.identifier.issnl1013-9923-

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