From the Departments of Neurosciences and Psychiatry (R.J.E.), University of California, San Diego; Sanford Burnham Prebys Medical Discovery Institute (S.N.P.); LECOM health - Millcreek Community Hospital (Y.L.), Erie, PA; Department of Pathology (R.S.), Department of Psychiatry (J.I., E.M., B.T., I.G., M.C.), and Departments of Medicine and Psychiatry (S.L.), University of California, San Diego.
Neurol Neuroimmunol Neuroinflamm. 2020 Jun 17;7(5). doi: 10.1212/NXI.0000000000000809. Print 2020 Sep.
To determine whether cannabis may reduce HIV-related persistent inflammation, we evaluated the relationship of cannabis use in people with HIV (PWH) to inflammatory cytokines in CSF and blood plasma.
We measured a panel of proinflammatory cytokines (interleukin [IL]-16, C-reactive protein [CRP], IL-6, interferon gamma-induced protein [IP]-10, soluble CD14, and soluble tumor necrosis factor receptor type II [sTNFRII]) in CSF and blood plasma in PWH and HIV- individuals who did or did not use cannabis at various levels of exposure. Participants in this observational cohort were recruited from community sources and underwent lumbar puncture and phlebotomy. Cannabis use parameters were characterized by self-report based on a semistructured timeline follow-back interview. Cytokines were measured using commercially available immunoassays. Data were analyzed using factor analysis.
Participants were 35 PWH and 21 HIV- individuals, mean (SD) age 45.4 (14.5) years, 41 cannabis ever users, and 15 never users. PWH and HIV- were not different in recency, cumulative months, grams, or density of cannabis use. A factor analysis using CSF biomarkers yielded a factor loading on CRP, IL-16, and sTNFRII that was significantly associated with recency of cannabis use (more recent use associated with lower factor 1 values, reflecting less inflammation; r = 0.331 [95% CI 0.0175, 0.586]). In particular, more recent cannabis use was related to lower IL-16 levels (r = 0.549 [0.282, 0.737]). Plasma biomarkers yielded a factor loading on sTNFRII and IP-10 that was associated with more recent cannabis use (more recent use related to less inflammation; r = 0.374 [0.0660, 0.617]).
Recent cannabis use was associated with lower levels of inflammatory biomarkers, both in CSF and blood, but in different patterns. These results are consistent with compartmentalization of immune effects of cannabis. The principal active components of cannabis are highly lipid soluble and sequestered in brain tissue; thus, our findings are consistent with specific anti-neuroinflammatory effects that may benefit HIV neurologic dysfunction.
为了确定大麻是否可以减轻与 HIV 相关的持续性炎症，我们评估了 HIV 感染者（PWH）中大麻使用与脑脊液和血浆中炎症细胞因子的关系。
我们测量了一组促炎细胞因子（白细胞介素[IL]-16、C 反应蛋白[CRP]、IL-6、干扰素γ诱导蛋白[IP]-10、可溶性 CD14 和可溶性肿瘤坏死因子受体 II 型[sTNFRII]）在 PWH 和 HIV-个体的脑脊液和血浆中的水平，这些个体在不同程度的暴露下使用或不使用大麻。这项观察性队列研究的参与者是从社区来源招募的，他们接受了腰椎穿刺和采血。大麻使用参数是通过基于半结构化时间线随访访谈的自我报告来描述的。细胞因子使用商业上可用的免疫测定法进行测量。使用因子分析进行数据分析。
参与者包括 35 名 PWH 和 21 名 HIV-个体，平均（SD）年龄为 45.4（14.5）岁，41 名大麻既往使用者和 15 名从未使用者。PWH 和 HIV-在最近使用、累积月数、克数或使用密度方面没有差异。使用 CSF 生物标志物进行的因子分析得出的 CRP、IL-16 和 sTNFRII 的因子负荷与大麻使用的最近时间显著相关（最近使用与较低的因子 1 值相关，反映出炎症程度较低；r = 0.331[95%CI 0.0175，0.586]）。特别是，最近使用大麻与较低的 IL-16 水平相关（r = 0.549[0.282，0.737]）。血浆生物标志物得出的 sTNFRII 和 IP-10 的因子负荷与最近使用大麻相关（最近使用与炎症程度较低相关；r = 0.374[0.0660，0.617]）。
最近使用大麻与脑脊液和血液中的炎症生物标志物水平降低有关，但模式不同。这些结果与大麻对免疫的分隔效应一致。大麻的主要活性成分具有高度脂溶性，被隔离在脑组织中；因此，我们的发现与可能有益于 HIV 神经功能障碍的特定抗神经炎症作用一致。
Zotero 插件
