Maternal exposure to ultrafine particles enhances influenza infection during pregnancy.
Maternal exposure to ultrafine particles enhances influenza infection during pregnancy.
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DOI：
10.1186/s12989-023-00521-1
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发表时间：
2023-04-17
影响因子：
10
通讯作者：
中科院分区：
文献类型：
--
作者：
空气污染和传染媒介之间的相互作用越来越被认识到，这对识别，特别是保护弱势群体至关重要。怀孕是流感感染和空气污染暴露的脆弱时期，但怀孕期间的相互作用仍不清楚。母体暴露于超细颗粒（UFP，100 nm直径），一类颗粒物质普遍存在于城市环境中，激发独特的肺部免疫反应。我们假设，妊娠期间暴露于UFP会导致对流感的异常免疫应答，从而增加感染的严重程度。 从我们充分表征的C57 Bl/6 N小鼠模型构建，采用从妊娠日（GD）0.5-13.5的每日妊娠UFP暴露，我们进行了初步研究，其中妊娠母鼠随后在GD 14.5感染流感A/波多黎各/8/1934（PR 8）。研究结果表明，PR 8感染导致过滤空气（FA）和UFP暴露组的体重增加减少。共同暴露于UFP和病毒感染导致PR 8病毒滴度显著升高并减少肺部炎症，这意味着先天性和适应性免疫防御的潜在抑制。在暴露于UFP并感染PR 8的妊娠小鼠中，前病毒因子鞘氨醇激酶1（Sphk 1）和促炎细胞因子白细胞介素-1 β（IL-1）的肺部表达显著增加;表达与较高的病毒滴度相关。我们的模型结果提供了初步的见解，了解孕妇在怀孕期间暴露于UFP如何增加呼吸道病毒感染的风险。该模型是建立未来监管和临床策略以保护暴露于UFP的孕妇的重要第一步。 在线版本包含补充材料，可通过10.1186/s12989-023-00521-1获得。
Interactions between air pollution and infectious agents are increasingly recognized and critical to identify, especially to protect vulnerable populations. Pregnancy represents a vulnerable period for influenza infection and air pollution exposure, yet interactions during pregnancy remain unclear. Maternal exposure to ultrafine particles (UFPs, 100 nm diameter), a class of particulate matter ubiquitous in urban environments, elicits unique pulmonary immune responses. We hypothesized that UFP exposure during pregnancy would lead to aberrant immune responses to influenza enhancing infection severity. Building from our well-characterized C57Bl/6N mouse model employing daily gestational UFP exposure from gestational day (GD) 0.5–13.5, we carried out a pilot study wherein pregnant dams were subsequently infected with Influenza A/Puerto Rico/8/1934 (PR8) on GD14.5. Findings indicate that PR8 infection caused decreased weight gain in filtered air (FA) and UFP-exposed groups. Co-exposure to UFPs and viral infection led to pronounced elevation in PR8 viral titer and reduced pulmonary inflammation, signifying potential suppression of innate and adaptive immune defenses. Pulmonary expression of the pro-viral factor sphingosine kinase 1 (Sphk1) and pro-inflammatory cytokine interleukin-1β (IL-1 ) was significantly increased in pregnant mice exposed to UFPs and infected with PR8; expression correlated with higher viral titer. Results from our model provide initial insight into how maternal UFP exposure during pregnancy enhances respiratory viral infection risk. This model is an important first step in establishing future regulatory and clinical strategies for protecting pregnant women exposed to UFPs. The online version contains supplementary material available at 10.1186/s12989-023-00521-1.
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