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Article: HIV-1 Tat dysregulation of lipopolysaccharide-induced cytokine responses: Microbial interactions in HIV infection

TitleHIV-1 Tat dysregulation of lipopolysaccharide-induced cytokine responses: Microbial interactions in HIV infection
Authors
KeywordsCytokines
Interferon
Lipopolysaccharides
Monocytes/macrophages
Tat
Issue Date2009
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.AIDSonline.com
Citation
Aids, 2009, v. 23 n. 12, p. 1473-1484 How to Cite?
AbstractOBJECTIVE: To examine whether the HIV-1 Tat protein impairs the lipopolysaccharide (LPS)-induced cytokine responses. DESIGN: Concurrent infections with pathogens including bacteria and viruses are common in AIDS patients. However, cytokine and interferon responses during infection with or translocation from the gut of these pathogens in HIV-infected patients are not well studied. As HIV-1 Tat contributes partly to the HIV-induced immune dysregulation, we investigated whether the protein may play a role in perturbing the LPS-induced cytokine responses. METHODS: Expression levels of cytokines in human primary blood monocytes/macrophages were determined by quantitative polymerase chain reaction and enzyme-linked immunosorbent assay. Expression level of the cell surface Toll-like receptor 4 was examined by flow cytometry. Activations of signaling molecules were assayed by western blot and immunofluorescence. RESULTS: We demonstrated that HIV-1 Tat downregulated the LPS-induction of IFN-β and concomitantly upregulated IL-6 expression in primary blood monocytes/macrophages, whereas the viral protein had no significant effects on TNF-α expression. To delineate the underlying mechanism, we showed that Tat inhibited the LPS-activation of ERK1/2 but not the p38 mitogen-activated protein kinases. The viral protein suppressed the LPS-induced activation of NFκB p65 via its induction of IκBα expression, which resulted in retention of NFκB p65 in the cytosol. CONCLUSION: These findings suggest that Tat may play a role in modulating the immune responses triggered by other coinfecting pathogens and thus providing a permissive environment for both HIV and other opportunistic microbes. © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Persistent Identifierhttp://hdl.handle.net/10722/79751
ISSN
2015 Impact Factor: 4.407
2015 SCImago Journal Rankings: 3.112
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYim, HCHen_HK
dc.contributor.authorLi, JCBen_HK
dc.contributor.authorLau, JSHen_HK
dc.contributor.authorLau, ASYen_HK
dc.date.accessioned2010-09-06T07:58:16Z-
dc.date.available2010-09-06T07:58:16Z-
dc.date.issued2009en_HK
dc.identifier.citationAids, 2009, v. 23 n. 12, p. 1473-1484en_HK
dc.identifier.issn0269-9370en_HK
dc.identifier.urihttp://hdl.handle.net/10722/79751-
dc.description.abstractOBJECTIVE: To examine whether the HIV-1 Tat protein impairs the lipopolysaccharide (LPS)-induced cytokine responses. DESIGN: Concurrent infections with pathogens including bacteria and viruses are common in AIDS patients. However, cytokine and interferon responses during infection with or translocation from the gut of these pathogens in HIV-infected patients are not well studied. As HIV-1 Tat contributes partly to the HIV-induced immune dysregulation, we investigated whether the protein may play a role in perturbing the LPS-induced cytokine responses. METHODS: Expression levels of cytokines in human primary blood monocytes/macrophages were determined by quantitative polymerase chain reaction and enzyme-linked immunosorbent assay. Expression level of the cell surface Toll-like receptor 4 was examined by flow cytometry. Activations of signaling molecules were assayed by western blot and immunofluorescence. RESULTS: We demonstrated that HIV-1 Tat downregulated the LPS-induction of IFN-β and concomitantly upregulated IL-6 expression in primary blood monocytes/macrophages, whereas the viral protein had no significant effects on TNF-α expression. To delineate the underlying mechanism, we showed that Tat inhibited the LPS-activation of ERK1/2 but not the p38 mitogen-activated protein kinases. The viral protein suppressed the LPS-induced activation of NFκB p65 via its induction of IκBα expression, which resulted in retention of NFκB p65 in the cytosol. CONCLUSION: These findings suggest that Tat may play a role in modulating the immune responses triggered by other coinfecting pathogens and thus providing a permissive environment for both HIV and other opportunistic microbes. © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.AIDSonline.comen_HK
dc.relation.ispartofAIDSen_HK
dc.rightsAIDS. Copyright © Lippincott Williams & Wilkins.en_HK
dc.subjectCytokinesen_HK
dc.subjectInterferonen_HK
dc.subjectLipopolysaccharidesen_HK
dc.subjectMonocytes/macrophagesen_HK
dc.subjectTaten_HK
dc.titleHIV-1 Tat dysregulation of lipopolysaccharide-induced cytokine responses: Microbial interactions in HIV infectionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0269-9370&volume=23&spage=1473&epage=84&date=2009&atitle=HIV-1+Tat+dysregulation+of+lipopolysaccharide-induced+cytokine+responses:+microbial+interactions+in+HIV+infectionen_HK
dc.identifier.emailLi, JCB: jamesli@hku.hken_HK
dc.identifier.emailLau, ASY: asylau@hku.hken_HK
dc.identifier.authorityLi, JCB=rp00496en_HK
dc.identifier.authorityLau, ASY=rp00474en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/QAD.0b013e32832d7abeen_HK
dc.identifier.pmid19622906en_HK
dc.identifier.scopuseid_2-s2.0-68649100230en_HK
dc.identifier.hkuros161096en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-68649100230&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume23en_HK
dc.identifier.issue12en_HK
dc.identifier.spage1473en_HK
dc.identifier.epage1484en_HK
dc.identifier.isiWOS:000268414300005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYim, HCH=15752404600en_HK
dc.identifier.scopusauthoridLi, JCB=23103447500en_HK
dc.identifier.scopusauthoridLau, JSH=40261886300en_HK
dc.identifier.scopusauthoridLau, ASY=7202626202en_HK

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