Center for Oral Health Research, College of Dentistry, University of Kentucky, Lexington, KY 40536, USA.
Immunology. 2011 Mar;132(3):401-9. doi: 10.1111/j.1365-2567.2010.03375.x. Epub 2010 Nov 12.
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.
由龈下生物膜组成的混合感染是引发牙周炎慢性免疫炎症病变的原因。这些微生物生物膜与宿主免疫细胞相互作用,随着疾病的进展而增加,可能导致 HIV-1 感染患者的 HIV 重新激活。先前的报告集中在单种细菌对巨噬细胞和树突状细胞的挑战能力,以详细描述它们的检测和信号通路的分子方面。本研究使用各种口腔细菌作为原型刺激物,对多细菌挑战下的巨噬细胞和树突状细胞的反应提供了开创性的描述,以检查这些反应特征。该研究采用 HIV 启动子激活和 HIV 病毒复制再激活的模型。与革兰氏阳性菌相比,口腔革兰氏阴性菌从所有细胞类型中引发 HIV 启动子激活和病毒复制的水平显著更高。口腔革兰氏阴性菌的选定组合在巨噬细胞和未成熟树突状细胞中引发 HIV 启动子激活和病毒复制的协同作用。在成熟树突状细胞中,HIV 启动子激活和病毒复制没有协同作用。在任何细胞模型中,革兰氏阳性菌都没有协同作用。这些发现支持确定多细菌对免疫细胞的影响和特征的重要性,以阐明口腔中可能发生的潜在免疫识别和抗原加工。