RSV是儿科的主要传染因子之一,它与空气污染的关系经常被观察到。然而,这种相互作用的分子基础报道很少。我们试图系统地回顾现有的文献,并确定知识空白来回答这个问题:空气污染物-RSV相互作用中隐含了哪些分子机制?在在线数据库中搜索了2022年8月之前发表的原始研究,重点是相互作用的分子机制。这些研究被绘制出来,叙事综合基于三个预期的影响方向:促进病毒进入,改变的病毒复制,和不适当的主机反应。我们确定了在1993年至2020年之间发表的25项研究(研究数量没有明显增加),这些研究是在人类中进行的(n=12)。动物(n=10)或混合(n=3)模型,并主要分析香烟烟雾(n=11),颗粒物(n=4),纳米粒子(n=3),和炭黑(n=2)。关于上皮屏障损伤的数据支持促进病毒进入的假设;一项研究还报道了在RSV与颗粒物缀合后加速病毒进入。空气污染可能导致坏死超过凋亡,and,作为一种效果,据报道病毒载量增加.同样,空气污染通过降低IFN-γ和Clara细胞分泌蛋白水平和降低的免疫反应来减轻上皮功能。由于肺泡巨噬细胞的病毒摄取减少和树突状细胞的功能受到抑制,免疫反应也可能减弱。另一方面,空气污染可能引发旺盛的炎症反应,并引起气道高反应性(AHR),肺浸润时间延长,和组织重塑,包括肺气肿的形成.AHR主要由IFN-γ和RANTES浓度增加介导,而肺气肿的风险与IL-17→MCP-1→MMP-9→MMP-12轴的激活有关。关于RSV-空气污染相互作用的分子基础的证据非常缺乏,这可能会对未来针对空气污染影响的行动提出严重问题。主要的知识差距涉及空气污染物(主要是香烟烟雾的影响被调查),促进急性感染或更严重疾病进程的机制(因为它可能有助于短期计划,尤其是非药理学的,干预措施),以及对感染反应不充分的机制(这可能导致急性感染的病程延长和长期后遗症)。到目前为止,关于相互作用的广泛性和复杂性的证据不足,未来的研究应该集中在各种空气污染物刺激的共同机制,以及不同浓度下不同污染物的影响比较。
RSV is one of the major infectious agents in paediatrics, and its relationship with air pollution is frequently observed. However, the molecular basis of this interaction is sparsely reported. We sought to systematically
review the existing body of literature and identify the knowledge gaps to answer the question: which molecular mechanisms are implied in the air pollutants-RSV interaction? Online databases were searched for original studies published before August 2022 focusing on molecular mechanisms of the interaction. The studies were charted and a narrative synthesis was based upon three expected directions of influence: a facilitated viral entry, an altered viral replication, and an inappropriate host reaction. We identified 25 studies published between 1993 and 2020 (without a noticeable increase in the number of studies) that were performed in human (n = 12), animal (n = 10) or mixed (n = 3) models, and analysed mainly cigarette smoke (n = 11), particulate matter (n = 4), nanoparticles (n = 3), and carbon black (n = 2). The data on a damage to the epithelial barrier supports the hypothesis of facilitated viral entry; one study also reported accelerated viral entry upon an RSV conjugation to particulate matter. Air pollution may result in the predominance of necrosis over apoptosis, and, as an effect, an increased viral load was reported. Similarly, air pollution mitigates epithelium function with decreased IFN-γ and Clara cell secretory protein levels and decreased immune response. Immune response might also be diminished due to a decreased viral uptake by alveolar macrophages and a suppressed function of dendritic cells. On the other hand, an exuberant inflammatory response might be triggered by air pollution and provoke airway hyperresponsiveness (AHR), prolonged lung infiltration, and tissue remodeling, including a formation of emphysema. AHR is mediated mostly by increased IFN-γ and RANTES concentrations, while the risk of emphysema was related to the activation of the IL-17 → MCP-1 → MMP-9 → MMP-12 axis. There is a significant lack of evidence on the molecular basics of the RSV-air pollution interaction, which may present a serious problem with regards to future actions against air pollution effects. The major knowledge gaps concern air pollutants (mostly the influence of cigarette smoke was investigated), the mechanisms facilitating an acute infection or a worse disease course (since it might help plan short-term, especially non-pharmacological, interventions), and the mechanisms of an inadequate response to the infection (which may lead to a prolonged course of an acute infection and long-term sequelae). Thus far, the evidence is insufficient regarding the broadness and complexity of the interaction, and future studies should focus on common mechanisms stimulated by various air pollutants and a comparison of influence of the different contaminants at various concentrations.