Lipid from electronic cigarette-aerosol both with and without nicotine induced pro-inflammatory macrophage polarization and disrupted phagocytosis.

IF 4.4 3区医学 Q2 IMMUNOLOGY

Journal of Inflammation-London Pub Date : 2023-11-17 DOI:10.1186/s12950-023-00367-6

Mizanur Rahman, Shanzina Iasmin Sompa, Micol Introna, Swapna Upadhyay, Koustav Ganguly, Lena Palmberg

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引用次数: 0

Abstract

Clinical cases and experimental evidence revealed that electronic cigarettes (ECIG) induce serious adverse health effects, but underlying mechanisms remain to be fully uncovered. Based on recent exploratory evidence, investigating the effects of ECIG on macrophages can broadly define potential mechanisms by focusing on the effect of ECIG exposure with or without nicotine. Here we investigated the effect of ECIG-aerosol exposure on macrophages (MQ) phenotype, inflammatory response, and function of macrophages.MQ were cultured at air liquid interface and exposed to ECIG-aerosol. Oxidative stress was determined by reactive oxygen species (ROS), heat shock protein 60 (HSP60), glutathione peroxidase (GPx) and heme oxygenase1 (HMOX1). Lipid accumulation and lipid peroxidation were defined by lipid staining and level of malondialdehyde (MDA) respectively. MQ polarization was identified by surface expression markers CD86, CD11C and CD206 as well as pro-inflammatory and anti-inflammatory cytokines in gene and protein level. Phagocytosis of E. coli by MQ was investigated by fluorescence-based phagocytosis assay.ECIG-aerosol exposure in presence or absence of nicotine induced oxidative stress evidenced by ROS, HSP60, GPx, GPx4 and HMOX1 upregulation in MQ. ECIG-aerosol exposure induced accumulation of lipids and the lipid peroxidation product MDA in MQ. Pro-inflammatory MQ (M1) markers CD86 and CD11C but not anti-inflammatory MQ (M2) marker CD206 were upregulated in response to ECIG-aerosol exposure. In addition, ECIG induced pro-inflammatory cytokines IL-1beta and IL-8 in gene level and IL-6, IL-8, and IL-1beta in protein level whereas ECIG exposure downregulated anti-inflammatory cytokine IL-10 in protein level. Phagocytosis activity of MQ was downregulated by ECIG exposure. shRNA mediated lipid scavenger receptor 'CD36' silencing inhibited ECIG-aerosol-induced pro-inflammatory MQ polarization and recovered phagocytic activity of MQ.ECIG exposure alters lung lipid homeostasis and thus induced inflammation by inducing M1 type MQ and impair phagocytic function, which could be a potential cause of ECIG-induced lung inflammation in healthy and inflammatory exacerbation in disease condition.

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含尼古丁和不含尼古丁的电子烟气雾剂中的脂质诱导促炎巨噬细胞极化和吞噬功能紊乱。

临床病例和实验证据表明，电子烟(ECIG)会引起严重的不良健康影响，但潜在的机制仍有待充分揭示。基于最近的探索性证据，研究ECIG对巨噬细胞的影响可以通过关注有或没有尼古丁的ECIG暴露的影响来广泛定义潜在的机制。在这里，我们研究了ecig气溶胶暴露对巨噬细胞(MQ)表型、炎症反应和功能的影响。MQ在气液界面培养，暴露于ecig -气溶胶中。采用活性氧(ROS)、热休克蛋白60 (HSP60)、谷胱甘肽过氧化物酶(GPx)和血红素加氧酶1 (HMOX1)测定氧化应激水平。脂质染色和丙二醛(MDA)水平分别定义脂质积累和脂质过氧化。通过表面表达标记CD86、CD11C和CD206以及促炎和抗炎细胞因子在基因和蛋白水平上鉴定MQ极化。采用荧光吞噬实验研究MQ对大肠杆菌的吞噬作用。通过MQ中ROS、HSP60、GPx、GPx4和HMOX1的上调来证明，暴露于ecig -气溶胶存在或不存在尼古丁诱导的氧化应激。ecig -气溶胶暴露诱导MQ脂质积累和脂质过氧化产物MDA。促炎MQ (M1)标记CD86和CD11C，但抗炎MQ (M2)标记CD206在ecig气溶胶暴露下上调。此外，ECIG在基因水平上诱导促炎因子il -1 β和IL-8，在蛋白水平上诱导IL-6、IL-8和il -1 β，而ECIG暴露在蛋白水平上下调抗炎因子IL-10。暴露于ECIG后，MQ的吞噬活性下调。shRNA介导的脂质清除受体CD36沉默抑制ecig气溶胶诱导的促炎MQ极化，恢复MQ的吞噬活性。ECIG暴露改变肺脂质稳态，从而通过诱导M1型MQ诱导炎症，损害吞噬功能，这可能是健康状态下ECIG诱导肺部炎症和疾病状态下炎症加剧的潜在原因。

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来源期刊

Journal of Inflammation-London IMMUNOLOGY-

CiteScore

7.90

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： Journal of Inflammation welcomes research submissions on all aspects of inflammation. The five classical symptoms of inflammation, namely redness (rubor), swelling (tumour), heat (calor), pain (dolor) and loss of function (functio laesa), are only part of the story. The term inflammation is taken to include the full range of underlying cellular and molecular mechanisms involved, not only in the production of the inflammatory responses but, more importantly in clinical terms, in the healing process as well. Thus the journal covers molecular, cellular, animal and clinical studies, and related aspects of pharmacology, such as anti-inflammatory drug development, trials and therapeutic developments. It also considers publication of negative findings. Journal of Inflammation aims to become the leading online journal on inflammation and, as online journals replace printed ones over the next decade, the main open access inflammation journal. Open access guarantees a larger audience, and thus impact, than any restricted access equivalent, and increasingly so, as the escalating costs of printed journals puts them outside University budgets. The unrestricted access to research findings in inflammation aids in promoting dynamic and productive dialogue between industrial and academic members of the inflammation research community, which plays such an important part in the development of future generations of anti-inflammatory therapies.