ABSTRACT
A massive depletion of CD4+ T lymphocytes has been described in early and acute human immunodeficiency virus (HIV) infection, leading to an imbalance between the human microbiome and immune responses. In recent years, a growing interest in the alterations in gut microbiota in HIV infection has led to many studies; however, only few studies have been conducted to explore the importance of oral microbiome in HIV-infected individuals. Evidence has indicated the dysbiosis of oral microbiota in people living with HIV (PLWH). Potential mechanisms might be related to the immunodeficiency in the oral cavity of HIV-infected individuals, including changes in secretory components such as reduced levels of enzymes and proteins in saliva and altered cellular components involved in the reduction and dysfunction of innate and adaptive immune cells. As a result, disrupted oral immunity in HIV-infected individuals leads to an imbalance between the oral microbiome and local immune responses, which may contribute to the development of HIV-related diseases and HIV-associated non-acquired immunodeficiency syndrome comorbidities. Although the introduction of antiretroviral therapy (ART) has led to a significant decrease in occurrence of the opportunistic oral infections in HIV-infected individuals, the dysbiosis in oral microbiome persists. Furthermore, several studies with the aim to investigate the ability of probiotics to regulate the dysbiosis of oral microbiota in HIV-infected individuals are ongoing. However, the effects of ART and probiotics on oral microbiome in HIV-infected individuals remain unclear. In this article, we review the composition of the oral microbiome in healthy and HIV-infected individuals and the possible effect of oral microbiome on HIV-associated oral diseases. We also discuss how ART and probiotics influence the oral microbiome in HIV infection. We believe that a deeper understanding of composition and function of the oral microbiome is critical for the development of effective preventive and therapeutic strategies for HIV infection.
Subject(s)
Humans , Dysbiosis , Gastrointestinal Microbiome , HIV Infections/drug therapy , Microbiota , MouthABSTRACT
<p><b>OBJECTIVE</b>In this review, to illustrate the resistance mechanism for pathogen insult, we discussed the role of the intestinal microbiome in promoting resistance to local gastrointestinal tract infections and to respiratory tract infections.</p><p><b>DATA SOURCES</b>The review was based on data obtained from the published research articles.</p><p><b>STUDY SELECTION</b>A total of 49 original articles were selected in accordance with our main objective to illustrate the resistance mechanism(s) by which commensal microbiota can contribute to host defense against local and systemic infections.</p><p><b>RESULTS</b>Diverse microorganisms colonize human environmentally exposed surfaces such as skin, respiratory tract, and gastrointestinal tract. Co-evolution has resulted in these microbes with extensive and diverse impacts on multiple aspects of host biological functions. During the last decade, high-throughput sequencing technology developed has been applied to study commensal microbiota and their impact on host biological functions. By using pathogen recognition receptors pathway and nucleotide binding oligomerization domain-like receptors pathway, the commensal microbiome promotes resistance to local and systemic infections, respectively. To protect against the local infections, the microbiome functions contain the following: the competing for sites of colonization, direct production of inhibition molecules or depletion of nutrients needed for pathogens, and priming immune defenses against pathogen insult. At the same time, with the purpose to maintain homeostasis, the commensal bacteria can program systemic signals toward not only local tissue but also distal tissue to modify their function for infections accordingly.</p><p><b>CONCLUSIONS</b>Commensal bacteria play an essential role in protecting against infections, shaping and regulating immune responses, and maintaining host immune homeostasis.</p>