The oral commensal, Streptococcus gordonii, synergizes with Tat protein to induce HIV-1 promoter activation in monocytes/macrophages

Octavio A. González; Jeffrey L. Ebersole; Chifu B. Huang

doi:10.1016/j.cellimm.2011.03.008

The oral commensal, Streptococcus gordonii, synergizes with Tat protein to induce HIV-1 promoter activation in monocytes/macrophages

Octavio A. González, Jeffrey L. Ebersole, Chifu B. Huang

Research output: Contribution to journal › Article › peer-review

2 Scopus citations

Abstract

Trans-activator of transcription (Tat) is an HIV-1 protein essential for viral replication. Oral periodontopathogens (e.g. Fusobacterium nucleatum) enhance HIV-1LTR promoter activation in monocytes/macrophages in absence of Tat; however, some oral commensals fail to trigger this response. We sought to determine the effect of Tat on HIV-1LTR promoter activation induced by the representative oral commensal Streptococcus gordonii in monocytes/macrophages. S. gordonii enhanced HIV-1LTR reactivation in THP89GFP (Tat⁺), but not in BF24 (Tat^-) cells. Interestingly, S. gordonii, but not Streptococcus sanguinis enhanced HIV-1LTR activation in the presence of recombinant Tat in BF24 cells. This response correlated with IL-8 but not TNFα or IL-6 production, and was abrogated by the NFκB inhibitor BAY 11-7082. Kinetics of NFκB-RelA activation did not explain the S. gordonii-induced HIV-1LTR activation in presence of Tat. These results suggest that S. gordonii-induced HIV-1 reactivation in monocytes/macrophages is Tat-dependent and appears to involve NFκB activation.

Original language	English
Pages (from-to)	38-45
Number of pages	8
Journal	Cellular Immunology
Volume	269
Issue number	1
DOIs	https://doi.org/10.1016/j.cellimm.2011.03.008
State	Published - 2011

Bibliographical note

Funding Information:
We give special thanks to Dr. David Levy from NYU for providing us the THP89GFP cell line. This study was supported by U.S.P.H.S. grant from the National Institute for Research Resources P20 RR020145 and funds from the University of Kentucky, College of Dentistry.

Keywords

HIV-1
Monocytes/macrophages
Oral bacteria
Periodontitis
S. gordonii
Transcriptional Trans-activator

ASJC Scopus subject areas

Immunology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.cellimm.2011.03.008

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@article{2f663733604e423f85d76ba1e78eed40,

title = "The oral commensal, Streptococcus gordonii, synergizes with Tat protein to induce HIV-1 promoter activation in monocytes/macrophages",

abstract = "Trans-activator of transcription (Tat) is an HIV-1 protein essential for viral replication. Oral periodontopathogens (e.g. Fusobacterium nucleatum) enhance HIV-1LTR promoter activation in monocytes/macrophages in absence of Tat; however, some oral commensals fail to trigger this response. We sought to determine the effect of Tat on HIV-1LTR promoter activation induced by the representative oral commensal Streptococcus gordonii in monocytes/macrophages. S. gordonii enhanced HIV-1LTR reactivation in THP89GFP (Tat+), but not in BF24 (Tat-) cells. Interestingly, S. gordonii, but not Streptococcus sanguinis enhanced HIV-1LTR activation in the presence of recombinant Tat in BF24 cells. This response correlated with IL-8 but not TNFα or IL-6 production, and was abrogated by the NFκB inhibitor BAY 11-7082. Kinetics of NFκB-RelA activation did not explain the S. gordonii-induced HIV-1LTR activation in presence of Tat. These results suggest that S. gordonii-induced HIV-1 reactivation in monocytes/macrophages is Tat-dependent and appears to involve NFκB activation.",

keywords = "HIV-1, Monocytes/macrophages, Oral bacteria, Periodontitis, S. gordonii, Transcriptional Trans-activator",

author = "Gonz{\'a}lez, {Octavio A.} and Ebersole, {Jeffrey L.} and Huang, {Chifu B.}",

note = "Funding Information: We give special thanks to Dr. David Levy from NYU for providing us the THP89GFP cell line. This study was supported by U.S.P.H.S. grant from the National Institute for Research Resources P20 RR020145 and funds from the University of Kentucky, College of Dentistry.",

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AU - González, Octavio A.

AU - Ebersole, Jeffrey L.

AU - Huang, Chifu B.

N1 - Funding Information: We give special thanks to Dr. David Levy from NYU for providing us the THP89GFP cell line. This study was supported by U.S.P.H.S. grant from the National Institute for Research Resources P20 RR020145 and funds from the University of Kentucky, College of Dentistry.

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AB - Trans-activator of transcription (Tat) is an HIV-1 protein essential for viral replication. Oral periodontopathogens (e.g. Fusobacterium nucleatum) enhance HIV-1LTR promoter activation in monocytes/macrophages in absence of Tat; however, some oral commensals fail to trigger this response. We sought to determine the effect of Tat on HIV-1LTR promoter activation induced by the representative oral commensal Streptococcus gordonii in monocytes/macrophages. S. gordonii enhanced HIV-1LTR reactivation in THP89GFP (Tat+), but not in BF24 (Tat-) cells. Interestingly, S. gordonii, but not Streptococcus sanguinis enhanced HIV-1LTR activation in the presence of recombinant Tat in BF24 cells. This response correlated with IL-8 but not TNFα or IL-6 production, and was abrogated by the NFκB inhibitor BAY 11-7082. Kinetics of NFκB-RelA activation did not explain the S. gordonii-induced HIV-1LTR activation in presence of Tat. These results suggest that S. gordonii-induced HIV-1 reactivation in monocytes/macrophages is Tat-dependent and appears to involve NFκB activation.

KW - HIV-1

KW - Monocytes/macrophages

KW - Oral bacteria

KW - Periodontitis

KW - S. gordonii

KW - Transcriptional Trans-activator

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The oral commensal, Streptococcus gordonii, synergizes with Tat protein to induce HIV-1 promoter activation in monocytes/macrophages

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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