» Articles » PMID: 21073452

Polybacterial Challenge Enhances HIV Reactivation in Latently Infected Macrophages and Dendritic Cells

Overview
Journal Immunology
Date 2010 Nov 16
PMID 21073452
Citations 7
Authors
Affiliations
Soon will be listed here.
Abstract

A polymicrobial infection comprising subgingival biofilms is the trigger for the chronic immunoinflammatory lesions of periodontitis. These microbial biofilms interface with host immune cells that increase with progressing disease and could result in HIV reactivation in HIV-1-infected patients. Previous reports have focused on the ability of monospecies challenge of macrophages and dendritic cells to detail molecular aspects of their detection and signalling pathways. This study provides a seminal description of the responses of macrophages and dendritic cells to a polybacterial challenge using various oral bacteria as prototype stimuli to examine these response characteristics. The investigation employed a model of HIV-promoter activation and reactivation of HIV viral replication. Oral Gram-negative bacteria elicited significantly greater levels of HIV promoter activation and viral replication from all cell types, compared with Gram-positive bacteria. Selected combinations of oral Gram-negative bacteria elicited synergistic HIV promoter activation and viral replication in macrophages and immature dendritic cells. In mature dendritic cells, there was no synergism in HIV promoter activation and viral replication. Gram-positive bacteria showed no synergism in any cell model. These findings support the importance of determining the characteristics and impact of polybacterial challenges on immune cells to clarify the potential immune recognition and antigen processing that can occur in the oral cavity.

Citing Articles

Current trends and new developments in HIV research and periodontal diseases.

Ryder M, Shiboski C, Yao T, Moscicki A Periodontol 2000. 2019; 82(1):65-77.

PMID: 31850628 PMC: 7441852. DOI: 10.1111/prd.12321.


Dendritic cells maturated by co-culturing with HIV-1 latently infected Jurkat T cells or stimulating with AIDS-associated pathogens secrete TNF-α to reactivate HIV-1 from latency.

Ren X, Ma L, Sun W, Kuang W, Li T, Jin X Virulence. 2017; 8(8):1732-1743.

PMID: 28762863 PMC: 5810491. DOI: 10.1080/21505594.2017.1356535.


Macrophage polarization in response to oral commensals and pathogens.

Huang C, Alimova Y, Ebersole J Pathog Dis. 2016; 74(3).

PMID: 26884502 PMC: 5975235. DOI: 10.1093/femspd/ftw011.


The macrophage: a therapeutic target in HIV-1 infection.

Kumar A, Herbein G Mol Cell Ther. 2015; 2:10.

PMID: 26056579 PMC: 4452058.


Oral innate immunity in HIV infection in HAART era.

Nittayananta W, Tao R, Jiang L, Peng Y, Huang Y J Oral Pathol Med. 2015; 45(1):3-8.

PMID: 25639844 PMC: 4671827. DOI: 10.1111/jop.12304.


References
1.
Lanzavecchia A, Sallusto F . Regulation of T cell immunity by dendritic cells. Cell. 2001; 106(3):263-6. DOI: 10.1016/s0092-8674(01)00455-x. View

2.
Kutsch O, Benveniste E, Shaw G, Levy D . Direct and quantitative single-cell analysis of human immunodeficiency virus type 1 reactivation from latency. J Virol. 2002; 76(17):8776-86. PMC: 136999. DOI: 10.1128/jvi.76.17.8776-8786.2002. View

3.
Frank I, Kacani L, Stoiber H, STOSSEL H, Spruth M, Steindl F . Human immunodeficiency virus type 1 derived from cocultures of immature dendritic cells with autologous T cells carries T-cell-specific molecules on its surface and is highly infectious. J Virol. 1999; 73(4):3449-54. PMC: 104111. DOI: 10.1128/JVI.73.4.3449-3454.1999. View

4.
Warger T, Osterloh P, Rechtsteiner G, Fassbender M, Heib V, Schmid B . Synergistic activation of dendritic cells by combined Toll-like receptor ligation induces superior CTL responses in vivo. Blood. 2006; 108(2):544-50. DOI: 10.1182/blood-2005-10-4015. View

5.
Paster B, Olsen I, Aas J, Dewhirst F . The breadth of bacterial diversity in the human periodontal pocket and other oral sites. Periodontol 2000. 2006; 42:80-7. DOI: 10.1111/j.1600-0757.2006.00174.x. View