电子烟的脂质-有或没有尼古丁的电子烟气溶诱导的炎症性巨细胞极化和破坏的细胞分裂
Mizanur Rahman1, Shanzina Iasmin Sompa2, Micol Introna2
1Unit of Integrative Toxicology, Institute of Environmental Medicine, Karolinska Institutet, 171 77, Stockholm, Sweden. mizanur.rahman@ki.se.
Journal of inflammation (London, England)
|November 18, 2023
概括
电子烟 (ECIG) 暴露会通过改变脂质新陈代谢和损害细胞形成,导致巨细胞 (MQ) 的氧化应激和炎症. 向CD36可能会减轻这些不良影响,为ECIG诱导的肺损伤提供了洞察力.
科学领域:
- 免疫学 免疫学 免疫学
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
背景情况:
- 电子烟 (ECIG) 与严重的不良健康影响有关,但根本机制尚未完全理解.
- 巨细胞 (MQ) 在肺免疫和炎症中起着至关重要的作用,使他们成为调查ECIG影响的关键目标.
- 研究ECIG对MQ表型,炎症和功能的影响可以阐明潜在的健康风险.
研究的目的:
- 研究ECIG气溶暴露对巨细胞表型,炎症反应和功能的影响.
- 确定氧化应激,脂质积累和极化在ECIG诱导的巨细胞变化的作用.
- 探索CD36在缓解ECIG诱导的巨细胞功能障碍方面的潜在治疗标.
主要方法:
- 在空气-液体界面培养的巨被暴露在含有或不含尼古丁的ECIG气溶中.
- 评估了氧化应激标志物 (ROS,HSP60,GPx,HMOX1),脂质积累 (脂质染色,MDA) 和MQ两极化 (CD86,CD11C,CD206,细胞因子).
- 使用基于光的测定来测量细胞活性,并通过shRNA沉默来研究CD36的作用.
主要成果:
- 暴露于ECIG气溶引起了氧化应激,脂质积累,并增加了促炎性M1巨标记物 (CD86,CD11C).
- 促炎性细胞因子 (IL-1β,IL-8,IL-6) 的上调,而抗炎性IL-10 的下调.
- 暴露于ECIG损害了巨细胞的细胞活性,通过沉默CD36部分恢复,表明其在ECIG诱导的炎症中的作用.
结论:
- 暴露于ECIG会破坏肺脂质平衡,促进M1巨细胞的两极分化,并损害食细胞功能.
- 这些变化有助于健康个体的ECIG诱导的肺炎,并加剧现有的炎症状况.
- 向CD36可能代表一种治疗策略,以抵消ECIG暴露对肺部健康的有害影响.
相关概念视频
Inflammation
53.6K
Overview
53.6K
Stimulants
218
Stimulants are substances that enhance neural activity and elevate dopamine levels in the brain, leading to their highly addictive nature. These drugs include cocaine, amphetamines, MDMA, caffeine, and nicotine, each with distinct mechanisms of action and varied health implications.
Cocaine can be administered via snorting, injection, or smoking. It primarily functions by blocking the reuptake of dopamine, resulting in a euphoric high characterized by an intense sensation of happiness and...
Cocaine can be administered via snorting, injection, or smoking. It primarily functions by blocking the reuptake of dopamine, resulting in a euphoric high characterized by an intense sensation of happiness and...
218
Chronic Obstructive Pulmonary Disease-II: Pathophysiology
2.8K
Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
Chronic Inflammation
2.8K


