INTRODUCTION Although detrimental effects of combustible cigarettes (CCs) on the progression of lung inflammatory diseases are well known, changes in electronic nicotine delivery systems (ENDS)-exposed lung-infiltrated immune cells are still unrevealed. AIMS AND METHODS The analysis of blood gas parameters, descriptive and quantitative histology of lung tissues, determination of serum cytokines, intracellular staining, and flow cytometry analysis of lung-infiltrated immune cells were used to determine the differences in the extent of lung injury and inflammation between mice from experimental (CC and ENDS-exposed animals) and control groups (Air-exposed mice). RESULTS Continuous exposition to either CCs or ENDS induced severe systemic inflammatory response, increased activation of NLRP3 inflammasome in neutrophils and macrophages and enhanced dendritic cell-dependent activation of Th1 and Th17 cells in the lungs. ENDS induced less severe immune response than CCs. Serum concentrations of inflammatory cytokines were significantly lower in the samples of ENDS-exposed mice. Compared to CCs, ENDS recruited lower number of circulating leukocytes in injured lungs and had less capacity to induce CD14/TLR2-dependent activation of NLRP3 inflammasome in lung-infiltrated neutrophils and macrophages. ENDS-primed dendritic cells had reduced capacity for the generation of Th1 and Th17 cell-driven lung inflammation. Accordingly, extensive immune cell-driven lung injury resulted in severe respiratory dysfunction in CCs-exposed mice, while ENDS caused moderate respiratory dysfunction in experimental animals. CONCLUSIONS Continuous exposition to either CCs or ENDS induced immune cell-driven lung damage in mice. ENDS triggered immune response, which was less potent than inflammatory response elicited by CCs and, therefore, caused less severe lung injury and inflammation. IMPLICATIONS This is the first study that compared the effects of CCs and ENDS on lung-infiltrated immune cells. Although both CCs and ENDS elicited systemic inflammatory response, immune cell-driven lung injury and inflammation were less severe in ENDS-exposed than in CC-exposed animals. Continuous exposition to ENDS-sourced aerosols was less harmful for respiratory function of experimental animals than CC-derived smoke.

中文翻译：

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可燃香烟和电子尼古丁输送系统对小鼠慢性肺部炎症发生和进展的影响。


引言 尽管可燃香烟（CC）对肺部炎症疾病进展的有害影响众所周知，但暴露于电子尼古丁输送系统（ENDS）的肺部浸润免疫细胞的变化仍未被揭示。目的和方法通过血气参数分析、肺组织描述性和定量组织学分析、血清细胞因子测定、细胞内染色以及肺浸润免疫细胞的流式细胞术分析来确定肺损伤和炎症程度的差异。实验组小鼠（接触 CC 和 ENDS 的动物）和对照组（接触空气的小鼠）之间的差异。结果 持续暴露于 CC 或 ENDS 会诱导严重的全身炎症反应，中性粒细胞和巨噬细胞中 NLRP3 炎症小体的激活增加，肺部 Th1 和 Th17 细胞的树突状细胞依赖性激活增强。 ENDS 诱导的免疫反应不如 CC 严重。在接触 ENDS 的小鼠样本中，炎症细胞因子的血清浓度显着降低。与CC相比，ENDS在受损肺部中募集的循环白细胞数量较少，并且在肺部浸润的中性粒细胞和巨噬细胞中诱导CD14/TLR2依赖性NLRP3炎症小体激活的能力较低。 ENDS 引发的树突状细胞产生 Th1 和 Th17 细胞驱动的肺部炎症的能力降低。因此，广泛的免疫细胞驱动的肺损伤导致接触 CC 的小鼠出现严重的呼吸功能障碍，而 ENDS 导致实验动物出现中度的呼吸功能障碍。结论 持续暴露于 CC 或 ENDS 会引起小鼠免疫细胞驱动的肺损伤。 ENDS 引发的免疫反应不如 CC 引起的炎症反应有效，因此引起的肺损伤和炎症较轻。意义 这是第一项比较 CC 和 ENDS 对肺部浸润免疫细胞影响的研究。尽管 CC 和 ENDS 都会引起全身炎症反应，但 ENDS 暴露的免疫细胞驱动的肺损伤和炎症比 CC 暴露的动物要轻。持续暴露于 ENDS 来源的气溶胶对实验动物呼吸功能的危害小于 CC 来源的烟雾。