Acute vaping in a golden Syrian hamster causes inflammatory response transcriptomic changes.
Acute vaping in a golden Syrian hamster causes inflammatory response transcriptomic changes.
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金色叙利亚仓鼠的急性吸电子烟导致炎症反应转录组变化。
DOI：
10.1152/ajplung.00162.2022
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发表时间：
2022
期刊：
影响因子：
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通讯作者：
White,CarlW
中科院分区：
文献类型：
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作者：
Hinds,DanielM;Nick,HeidiJ;Vallin,TessaM;Bloomquist,LeslieA;Christeson,Sarah;Bratcher,PrestonE;Cooper,EmilyH;Brinton,JohnT;Bosco-Lauth,Angela;White,CarlW
电子烟蒸发是尼古丁消费的一个主要方面，特别是对儿童和年轻人来说。尽管电子烟被认为是吸烟的更安全的替代品，但亚急性和慢性电子烟蒸发暴露的小鼠和大鼠模型显示出呼吸道的许多促炎变化。在金黄的叙利亚仓鼠身上还没有证明急性蒸发暴露的范例，而仓鼠是一种容易获得的小动物模型，它具有感染和传播呼吸道病毒(包括SARS-CoV-2)的独特好处，而不需要改变动物或病毒的基因。采用为期2天的雄性金黄地鼠全身蒸发暴露方案，通过逆转录定量聚合酶链式反应(RT-qPCR)检测血清可替宁、支气管肺泡灌洗细胞、肺和鼻腔组织病理学改变，以及鼻咽和肺组织中基因的表达。根据非正态或异常值的存在，采用方差分析或Kruskal-Wallis检验进行统计分析。对于有统计学意义的检验(P<；0.05)，分别进行组间比较后的Tukey-Kramer检验和Dunn‘s检验。在鼻组织中，RT-qPCR分析显示与1型炎症(CCL-5和CXCL-10)、纤维化[转化生长因子-β(转化生长因子-β)]、尼古丁非依赖性氧化应激反应(SOD2)和尼古丁非依赖性血管生成/血管生成(VEGFA)相关的基因表达增加。在肺中，涉及肾素-血管紧张素途径[血管紧张素转换酶，血管紧张素转换酶]，凝血因子，细胞外基质重塑，1型炎症(IL-1β，肿瘤坏死因子-α和CXCL-10)，纤维化(转化生长因子-β和丝裂原-1)，氧化应激反应(超氧化物歧化酶-2)，中性粒细胞细胞外陷阱释放(ELANE)，血管生成和血管生成(血管生成和血管生成)相关基因的表达在尼古丁依赖下增加。据我们所知，这是第一次证明叙利亚仓鼠是电子烟蒸发的可行模型。此外，这是第一个关于电子烟中尼古丁的蒸发可以增加肺组织因子基因表达的报道。我们的结果表明，即使是急性暴露在电子烟蒸发中，也会导致呼吸道中mRNAs的显著上调，这些途径涉及肾素-血管紧张素系统、凝血、细胞外基质重构、1型炎症、纤维化、氧化应激反应、中性粒细胞外陷阱释放(NETsis)、血管生成和血管生成。
E-cigarette vaping is a major aspect of nicotine consumption, especially for children and young adults. Although it is branded as a safer alternative to cigarette smoking, murine and rat models of subacute and chronic e-cigarette vaping exposure have shown many proinflammatory changes in the respiratory tract. An acute vaping exposure paradigm has not been demonstrated in the golden Syrian hamster, and the hamster is a readily available small animal model that has the unique benefit of becoming infected with and transmitting respiratory viruses, including SARS-CoV-2, without genetic alteration of the animal or virus. Using a 2-day, whole body vaping exposure protocol in male golden Syrian hamsters, we evaluated serum cotinine, bronchoalveolar lavage cells, lung, and nasal histopathology, and gene expression in the nasopharynx and lung through reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Depending on the presence of nonnormality or outliers, statistical analysis was performed by ANOVA or Kruskal–Wallis tests. For tests that were statistically significant (P< 0.05), post hoc Tukey–Kramer and Dunn’s tests, respectively, were performed to make pairwise comparisons between groups. In nasal tissue, RT-qPCR analysis revealed nicotine-dependent increases in gene expression associated with type 1 inflammation (CCL-5andCXCL-10), fibrosis [transforming growth factor-β (TGF-β)], nicotine-independent increase oxidative stress response (SOD-2), and a nicotine-independent decrease in vasculogenesis/angiogenesis (VEGF-A). In the lung, nicotine-dependent increases in the expression of genes involved in the renin-angiotensin pathway [angiotensin-converting enzyme (ACE),ACE2], coagulation (tissue factor,Serpine-1), extracellular matrix remodeling (MMP-2,MMP-9), type 1 inflammation (IL-1β,TNF-α, andCXCL-10), fibrosis (TGF-βandSerpine-1), oxidative stress response (SOD-2), neutrophil extracellular traps release (ELANE), and vasculogenesis and angiogenesis (VEGF-A) were identified. To our knowledge, this is the first demonstration that the Syrian hamster is a viable model of e-cigarette vaping. In addition, this is the first report that e-cigarette vaping with nicotine can increasetissue factorgene expression in the lung. Our results show that even an acute exposure to e-cigarette vaping causes significant upregulation of mRNAs in the respiratory tract from pathways involving the renin-angiotensin system, coagulation, extracellular matrix remodeling, type 1 inflammation, fibrosis, oxidative stress response, neutrophil extracellular trap release (NETosis), vasculogenesis, and angiogenesis.