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HIV感染与黏膜免疫受损:口腔表现与全身炎症

HIV Infection and Compromised Mucosal Immunity: Oral Manifestations and Systemic Inflammation.

作者信息

Heron Samantha E, Elahi Shokrollah

机构信息

Faculty of Medicine and Dentistry, Department of Dentistry, University of Alberta , Edmonton, AB , Canada.

Faculty of Medicine and Dentistry, Department of Dentistry, University of Alberta, Edmonton, AB, Canada; Faculty of Medicine and Dentistry, Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, AB, Canada.

出版信息

Front Immunol. 2017 Mar 7;8:241. doi: 10.3389/fimmu.2017.00241. eCollection 2017.

DOI:10.3389/fimmu.2017.00241
PMID:28326084
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5339276/
Abstract

Mucosal surfaces account for the vast majority of HIV transmission. In adults, HIV transmission occurs mainly by vaginal and rectal routes but rarely oral route. By contrast, pediatric HIV infections could be as the result of oral route by breastfeeding. As such mucosal surfaces play a crucial role in HIV acquisition, and spread of the virus depends on its ability to cross a mucosal barrier. HIV selectively infects, depletes, and/or dysregulates multiple arms of the human immune system particularly at the mucosal sites and causes substantial irreversible damage to the mucosal barriers. This leads to microbial products translocation and subsequently hyper-immune activation. Although introduction of antiretroviral therapy (ART) has led to significant reduction in morbidity and mortality of HIV-infected patients, viral replication persists. As a result, antigen presence and immune activation are linked to "inflammaging" that attributes to a pro-inflammatory environment and the accelerated aging process in HIV patients. HIV infection is also associated with the prevalence of oral mucosal infections and dysregulation of oral microbiota, both of which may compromise the oral mucosal immunity of HIV-infected individuals. In addition, impaired oral immunity in HIV infection may predispose the patients to periodontal diseases that are associated with systemic inflammation and increased risk of cardiovascular diseases. The purpose of this review is to examine existing evidence regarding the role of innate and cellular components of the oral cavity in HIV infection and how HIV infection may drive systemic hyper-immune activation in these patients. We will also discuss current knowledge on HIV oral transmission, HIV immunosenescence in relation to the oral mucosal alterations during the course of HIV infection and periodontal disease. Finally, we discuss oral manifestations associated with HIV infection and how HIV infection and ART influence the oral microbiome. Therefore, unraveling how HIV compromises the integrity of the oral mucosal tissues and innate immune components of the oral cavity and its association with induction of chronic inflammation are critical for the development of effective preventive interventions and therapeutic strategies.

摘要

黏膜表面是绝大多数HIV传播的途径。在成年人中,HIV主要通过阴道和直肠途径传播,但经口腔途径传播的情况很少见。相比之下,儿童HIV感染可能是通过母乳喂养经口腔途径传播所致。因此,黏膜表面在HIV感染过程中起着至关重要的作用,病毒的传播取决于其跨越黏膜屏障的能力。HIV选择性地感染、消耗和/或失调人体免疫系统的多个分支,尤其是在黏膜部位,并对黏膜屏障造成严重的不可逆损害。这会导致微生物产物易位,进而引发过度免疫激活。尽管抗逆转录病毒疗法(ART)的引入显著降低了HIV感染患者的发病率和死亡率,但病毒复制仍持续存在。结果,抗原的存在和免疫激活与“炎症衰老”相关,这导致了HIV患者体内的促炎环境和加速衰老过程。HIV感染还与口腔黏膜感染的流行以及口腔微生物群失调有关,这两者都可能损害HIV感染者的口腔黏膜免疫力。此外,HIV感染导致的口腔免疫力受损可能使患者易患与全身炎症和心血管疾病风险增加相关的牙周疾病。本综述的目的是研究现有证据,探讨口腔固有成分和细胞成分在HIV感染中的作用,以及HIV感染如何在这些患者中引发全身过度免疫激活。我们还将讨论关于HIV经口腔传播、HIV免疫衰老与HIV感染过程中口腔黏膜改变及牙周疾病的关系的现有知识。最后,我们将讨论与HIV感染相关的口腔表现,以及HIV感染和ART如何影响口腔微生物群。因此,弄清楚HIV如何破坏口腔黏膜组织的完整性和口腔固有免疫成分,以及其与慢性炎症诱导的关联,对于制定有效的预防干预措施和治疗策略至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3ad/5339276/17110c0d1734/fimmu-08-00241-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3ad/5339276/5667f013a3ca/fimmu-08-00241-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3ad/5339276/83d69fd1d12f/fimmu-08-00241-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3ad/5339276/17110c0d1734/fimmu-08-00241-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3ad/5339276/5667f013a3ca/fimmu-08-00241-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3ad/5339276/83d69fd1d12f/fimmu-08-00241-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3ad/5339276/17110c0d1734/fimmu-08-00241-g003.jpg

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