Center for Substance Abuse Research, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA.
Center for Substance Abuse Research, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA.
Brain Behav Immun. 2024 Mar;117:100-111. doi: 10.1016/j.bbi.2024.01.001. Epub 2024 Jan 8.
Oxycodone is the most prescribed opioid for pain management and has been available in clinics for almost a century, but effects of chronic oxycodone have been studied less than morphine in preclinical and clinical studies. Newly developed depression has been coupled with chronic oxycodone use in a few clinical studies, but no preclinical studies have investigated the pathogenesis of oxycodone-induced depression. Gut microbiome changes following oxycodone use is an understudied area, and interleukin-17A (IL-17A) is linked to both the development of mood disorders and regulation of gut microbiome. The present study investigated effects of chronic oxycodone exposure on mood-related behaviors (depression and anxiety), pain hypersensitivity, physical dependence, immune markers, and the gut microbiome and tested the hypothesis that blocking IL-17A with a systemically administered monoclonal antibody reduces oxycodone-derived effects. Oxycodone (using an incremental dosing regimen) or saline was injected twice a day for 12 days. IL-17A Ab (200 µg/100 µl) or saline was administered every 3rd day during the 12-day interval. Chronic oxycodone induced a depression-like effect, but not anxiogenic- or anxiolytic-like effects; promoted hyperalgesia; increased IL-17A and IL-6 levels in the ventral tegmental area (VTA); and induced physical dependence. IL-17A Ab co-administration with oxycodone prevented the depression-like effect and hyperalgesia, reduced naloxone-precipitated withdrawal signs, and normalized the increase in cytokine levels. Chronic oxycodone exposure did not affect gut microbiome and integrity. Our results identify a role for IL-17A in oxycodone-related behavioral and neuroimmune effects and show that IL-17A Ab has potential therapeutic value in blocking these effects. Given that humanized IL-17A Ab is approved for treatment of psoriasis and psoriatic arthritis, our findings point toward studying it for use in the treatment of oxycodone use disorder.
羟考酮是用于疼痛管理的最常开的阿片类药物,在临床中已有近一个世纪的应用,但在临床前和临床研究中,对慢性羟考酮的作用研究少于吗啡。在一些临床研究中,新出现的抑郁与慢性羟考酮的使用有关,但没有临床前研究调查羟考酮引起的抑郁的发病机制。羟考酮使用后的肠道微生物组变化是一个研究不足的领域,白细胞介素-17A(IL-17A)与情绪障碍的发展和肠道微生物组的调节有关。本研究调查了慢性羟考酮暴露对与情绪相关的行为(抑郁和焦虑)、疼痛过敏、身体依赖、免疫标志物以及肠道微生物组的影响,并检验了用系统给予单克隆抗体阻断 IL-17A 可减少羟考酮衍生作用的假说。用递增剂量方案每天两次注射羟考酮(或生理盐水)共 12 天。在 12 天的间隔内,每隔 3 天给予 IL-17A Ab(200μg/100μl)或生理盐水。慢性羟考酮引起类似抑郁的作用,但没有引起焦虑样或抗焦虑样作用;促进痛觉过敏;增加腹侧被盖区(VTA)的 IL-17A 和 IL-6 水平;并诱导身体依赖。IL-17A Ab 与羟考酮共同给药可预防类似抑郁的作用和痛觉过敏,减少纳洛酮诱发的戒断症状,并使细胞因子水平的升高正常化。慢性羟考酮暴露不影响肠道微生物组和完整性。我们的结果表明,IL-17A 在羟考酮相关的行为和神经免疫作用中起作用,并表明 IL-17A Ab 在阻断这些作用方面具有潜在的治疗价值。鉴于人源化 IL-17A Ab 已被批准用于治疗银屑病和银屑病关节炎,我们的发现表明,研究其用于治疗羟考酮使用障碍具有重要意义。