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.
|Number of pages||8|
|State||Published - 2011|
Bibliographical noteFunding 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.
- Oral bacteria
- S. gordonii
- Transcriptional Trans-activator
ASJC Scopus subject areas