HIV-Associated Interactions Between Oral Microbiota and Mucosal Immune Cells: Knowledge Gaps and Future Directions.
HIV-Associated Interactions Between Oral Microbiota and Mucosal Immune Cells: Knowledge Gaps and Future Directions.
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DOI：
10.3389/fimmu.2021.676669
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发表时间：
2021
影响因子：
7.3
通讯作者：
Garzino-Demo A
中科院分区：
文献类型：
--
作者：
Coker MO;Cairo C;Garzino-Demo A
即使持续使用抗逆转录病毒治疗（ART），HIV感染者也会增加全身共病和口腔病理的风险，包括机会性感染、口腔粘膜炎症以及牙龈和牙周疾病。在持续抑制病毒的情况下，导致这种风险增加的免疫介导机制尚不清楚。HIV感染，即使得到控制，也会改变微生物群落，导致慢性低度炎症状态，这是这些非HIV合并症的基础。在接受抗逆转录病毒治疗的艾滋病毒感染者中，龋齿、粘膜和牙周炎症的患病率较高，这通常与口腔微生物群落的丰度差异有关，可能导致对炎症的易感性增加。这篇小型综述强调了目前关于微生物介导的口腔粘膜免疫与艾滋病毒感染的知识差距，同时讨论了未来研究调查和实施新方法来阐明这些差距的机会。需要针对炎症和微生物多样性的干预措施来减轻口腔炎症相关的合并症，特别是在HIV感染者中。更广泛地说，需要更多的研究来支持微生物组介导的慢性免疫激活的一般模型，并帮助开发精确的微生物组靶向干预措施，以逆转或减轻不良后果。
Even with sustained use of antiretroviral therapy (ART), HIV-infected individuals have an increased risk of systemic comorbid conditions and oral pathologies, including opportunistic infections, oral mucosal inflammation, and gingival and periodontal diseases. The immune-mediated mechanisms that drive this increased risk, in the context of sustained viral suppression, are unclear. HIV infection, even when controlled, alters microbial communities contributing to a chronic low-grade inflammatory state that underlies these non-HIV co-morbidities. The higher prevalence of dental caries, and mucosal and periodontal inflammation reported in HIV-infected individuals on ART is often associated with differentially abundant oral microbial communities, possibly leading to a heightened susceptibility to inflammation. This mini-review highlights current gaps in knowledge regarding the microbe-mediated oral mucosal immunity with HIV infection while discussing opportunities for future research investigations and implementation of novel approaches to elucidate these gaps. Interventions targeting both inflammation and microbial diversity are needed to mitigate oral inflammation-related comorbidities, particularly in HIV-infected individuals. More broadly, additional research is needed to bolster general models of microbiome-mediated chronic immune activation and aid the development of precise microbiota-targeted interventions to reverse or mitigate adverse outcomes.
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影响因子：
3.7
作者：
Eberhard JM;Hartjen P;Kummer S;Schmidt RE;Bockhorn M;Lehmann C;Balagopal A;Hauber J;van Lunzen J;Schulze zur Wiesch J
通讯作者：
Schulze zur Wiesch J
影响因子：
7.3
作者：
Greenspan NS
通讯作者：
Greenspan NS
影响因子：
3.6
作者：
Coker, Modupe;El-Kamary, Samer S.;Charurat, Manhattan
通讯作者：
Charurat, Manhattan
影响因子：
--
作者：
Burne, R A
通讯作者：
Burne, R A
影响因子：
3.6
作者：
Blignaut, Elaine;Rossouw, Theresa M.;Feucht, Ute D.
通讯作者：
Feucht, Ute D.