The impact of cannabinoids on inflammasome signaling in HIV-1 infection.

NeuroImmune pharmacology and therapeutics Pub Date : 2023-03-25 Epub Date: 2023-02-23 DOI:10.1515/nipt-2023-0002
Alice K Min, Aislinn M Keane, Matthew Paltiel Weinstein, Talia H Swartz
{"title":"The impact of cannabinoids on inflammasome signaling in HIV-1 infection.","authors":"Alice K Min, Aislinn M Keane, Matthew Paltiel Weinstein, Talia H Swartz","doi":"10.1515/nipt-2023-0002","DOIUrl":null,"url":null,"abstract":"<p><p>Human immunodeficiency virus type 1 (HIV-1) is a chronic disease that afflicts over 38 million people worldwide without a known cure. The advent of effective antiretroviral therapies (ART) has significantly decreased the morbidity and mortality associated with HIV-1 infection in people living with HIV-1 (PWH), thanks to durable virologic suppression. Despite this, people with HIV-1 experience chronic inflammation associated with co-morbidities. While no single known mechanism accounts for chronic inflammation, there is significant evidence to support the role of the NLRP3 inflammasome as a key driver. Numerous studies have demonstrated therapeutic impact of cannabinoids, including exerting modulatory effects on the NLRP3 inflammasome. Given the high rates of cannabinoid use in PWH, it is of great interest to understand the intersecting biology of the role of cannabinoids in HIV-1-associated inflammasome signaling. Here we describe the literature of chronic inflammation in people with HIV, the therapeutic impact of cannabinoids in PWH, endocannabinoids in inflammation, and HIV-1-associated inflammation. We describe a key interaction between cannabinoids, the NLRP3 inflammasome, and HIV-1 viral infection, which supports further investigation of the critical role of cannabinoids in HIV-1 infection and inflammasome signaling.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"2 1","pages":"79-88"},"PeriodicalIF":0.0000,"publicationDate":"2023-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10070009/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"NeuroImmune pharmacology and therapeutics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1515/nipt-2023-0002","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/2/23 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Human immunodeficiency virus type 1 (HIV-1) is a chronic disease that afflicts over 38 million people worldwide without a known cure. The advent of effective antiretroviral therapies (ART) has significantly decreased the morbidity and mortality associated with HIV-1 infection in people living with HIV-1 (PWH), thanks to durable virologic suppression. Despite this, people with HIV-1 experience chronic inflammation associated with co-morbidities. While no single known mechanism accounts for chronic inflammation, there is significant evidence to support the role of the NLRP3 inflammasome as a key driver. Numerous studies have demonstrated therapeutic impact of cannabinoids, including exerting modulatory effects on the NLRP3 inflammasome. Given the high rates of cannabinoid use in PWH, it is of great interest to understand the intersecting biology of the role of cannabinoids in HIV-1-associated inflammasome signaling. Here we describe the literature of chronic inflammation in people with HIV, the therapeutic impact of cannabinoids in PWH, endocannabinoids in inflammation, and HIV-1-associated inflammation. We describe a key interaction between cannabinoids, the NLRP3 inflammasome, and HIV-1 viral infection, which supports further investigation of the critical role of cannabinoids in HIV-1 infection and inflammasome signaling.

Abstract Image

Abstract Image

大麻素对 HIV-1 感染中炎性信号转导的影响。
1 型人类免疫缺陷病毒(HIV-1)是一种慢性疾病,困扰着全球 3800 多万人,目前尚无治愈方法。有效的抗逆转录病毒疗法(ART)的出现大大降低了 HIV-1 感染者(PWH)的发病率和死亡率,这要归功于持久的病毒抑制。尽管如此,HIV-1 感染者仍会经历与并发症相关的慢性炎症。虽然没有单一的已知机制可以解释慢性炎症,但有大量证据支持 NLRP3 炎症小体是一个关键的驱动因素。大量研究证明了大麻素的治疗作用,包括对 NLRP3 炎症小体的调节作用。鉴于 PWH 中大麻素的高使用率,了解大麻素在 HIV-1 相关炎性体信号转导中的交叉生物学作用具有重大意义。在此,我们将介绍有关 HIV 感染者慢性炎症、大麻素对 PWH 的治疗影响、炎症中的内源性大麻素以及 HIV-1 相关炎症的文献。我们描述了大麻素、NLRP3 炎症小体和 HIV-1 病毒感染之间的关键相互作用,这支持进一步研究大麻素在 HIV-1 感染和炎症小体信号转导中的关键作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信