| HIV-1 reactivation induced by the periodontal pathogens Fusobacterium nucleatum and Porphyromonas gingivalis involves Toll-like receptor 2 [corrected] and 9 activation in monocytes/macrophages. | |
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MedLine Citation:
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PMID: 20610663 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Although oral coinfections (e.g., periodontal disease) are highly prevalent in human immunodeficiency virus type 1-positive (HIV-1(+)) patients and appear to positively correlate with viral load levels, the potential for oral bacteria to induce HIV-1 reactivation in latently infected cells has received little attention. We showed that HIV-1 long terminal repeat (LTR) promoter activation can be induced by periodontopathogens in monocytes/macrophages; nevertheless, the mechanisms involved in this response remain undetermined. Since Toll-like receptor 2 (TLR2), TLR4, and TLR9 activation have been involved in HIV-1 recrudescence, we sought to determine the role of these TLRs in HIV-1 reactivation induced by the periodontal pathogens Fusobacterium nucleatum and Porphyromonas gingivalis using BF24 monocytes/macrophages stably transfected with the HIV-1 promoter driving chloramphenicol acetyltransferase (CAT) expression and THP89GFP cells, a model of HIV-1 latency. We demonstrated that TLR9 activation by F. nucleatum and TLR2 activation by both bacteria appear to be involved in HIV-1 reactivation; however, TLR4 activation had no effect. Moreover, the autocrine activity of tumor necrosis factor alpha (TNF-alpha) but not interleukin-1beta (IL-1beta) produced in response to bacteria could impact viral reactivation. The transcription factors NF-kappaB and Sp1 appear to be positively regulating HIV-1 reactivation induced by these oral pathogens. These results suggest that oral Gram-negative bacteria (F. nucleatum and P. gingivalis) associated with oral and systemic chronic inflammatory disorders enhance HIV-1 reactivation in monocytes/macrophages through TLR2 and TLR9 activation in a mechanism that appears to be transcriptionally regulated. Increased bacterial growth and emergence of these bacteria or their products accompanying chronic oral inflammatory diseases could be risk modifiers for viral replication, systemic immune activation, and AIDS progression in HIV-1(+) patients. |
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Authors:
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Octavio A González; Mengtao Li; Jeffrey L Ebersole; Chifu B Huang |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. Date: 2010-07-07 |
Journal Detail:
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Title: Clinical and vaccine immunology : CVI Volume: 17 ISSN: 1556-679X ISO Abbreviation: Clin. Vaccine Immunol. Publication Date: 2010 Sep |
Date Detail:
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Created Date: 2010-09-02 Completed Date: 2010-12-08 Revised Date: 2011-07-25 |
Medline Journal Info:
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Nlm Unique ID: 101252125 Medline TA: Clin Vaccine Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 1417-27 Citation Subset: IM |
Affiliation:
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Center for Oral Health Research, College of Dentistry, University of Kentucky, Lexington, KY 40536-0305, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Cell Line Fusobacterium nucleatum / immunology*, pathogenicity HIV-1 / immunology, pathogenicity* Humans Interleukin-1beta / metabolism Monocytes / immunology, virology* NF-kappa B / metabolism Porphyromonas gingivalis / immunology*, pathogenicity Sp1 Transcription Factor / metabolism Toll-Like Receptor 2 / immunology* Toll-Like Receptor 4 / immunology Toll-Like Receptor 9 / immunology* Tumor Necrosis Factor-alpha / metabolism Virus Activation* |
| Grant Support | |
ID/Acronym/Agency:
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P20 RR020145/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Interleukin-1beta; 0/NF-kappa B; 0/Sp1 Transcription Factor; 0/Toll-Like Receptor 2; 0/Toll-Like Receptor 4; 0/Toll-Like Receptor 9; 0/Tumor Necrosis Factor-alpha |
| Comments/Corrections | |
Erratum In:
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Clin Vaccine Immunol. 2010 Nov;17(11):1825 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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