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, $$\le$$ 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 $$\beta$$ ) 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.

中文翻译：

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母亲暴露于超细颗粒会增加怀孕期间的流感感染

空气污染与传染源之间的相互作用越来越受到认可，并且对其识别至关重要，尤其是对于保护弱势群体而言。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。母亲暴露于超细颗粒物（UFP，直径 $$\le$$ 100 nm）是一类在城市环境中普遍存在的颗粒物，会引发独特的肺部免疫反应。我们假设在怀孕期间接触 UFP 会导致对流感的异常免疫反应，从而增加感染的严重程度。从我们充分表征的 C57Bl/6N 小鼠模型构建，使用从妊娠日 (GD) 0.5–13.5 开始的每日妊娠 UFP 暴露，我们开展了一项试点研究，其中怀孕的母鼠随后在 GD14.5 感染了甲型流感/波多黎各/8/1934 (PR8)。研究结果表明，PR8 感染导致过滤空气 (FA) 和 UFP 暴露组的体重增加减少。同时暴露于 UFP 和病毒感染导致 PR8 病毒滴度显着升高并减少肺部炎症，这表明先天和适应性免疫防御可能受到抑制。在暴露于 UFP 并感染 PR8 的怀孕小鼠中，促病毒因子鞘氨醇激酶 1 (Sphk1) 和促炎细胞因子白细胞介素 1β (IL-1 $$\beta$$) 的肺部表达显着增加；表达与较高的病毒滴度相关。我们模型的结果提供了关于孕期母体 UFP 暴露如何增加呼吸道病毒感染风险的初步见解。