Exposure to environmental geogenic (or earth-derived) dust can lead to more frequent and severe infections in the human airway. Particulate matter < 10 µm (PM₁₀) is the component of air pollution that is commonly associated with the exacerbation of respiratory diseases. We have previously demonstrated that mice exposed to geogenic dust PM₁₀ experienced an exacerbation of inflammatory responses to influenza A virus. Whether geogenic dust PM₁₀ also exacerbates respiratory bacterial infection is not yet known, nor are the components of the dust that drive these responses.

We treated airway bronchial epithelial cells (NuLi-1) with UV-irradiated geogenic dust PM₁₀ from six remote Western Australian towns. High levels of IL-6 and IL-8 production were observed, as well as persistent microbial growth. 16 S rRNA sequencing of the growth identified the microbe as Bacillus licheniformis, a spore-forming, environmentally abundant bacterium. We next investigated the interaction of B. licheniformis with respiratory epithelium in vitro to determine whether this exacerbated infection with a bacterial respiratory pathogen (non-typeable Haemophilus influenzae, NTHi).

Heat treatment (100 °C) of all PM₁₀ samples eliminated B. licheniformis contamination and reduced epithelial inflammatory responses, suggesting that heat-labile and/or microbial factors were involved in the host response to geogenic dust PM₁₀. We then exposed NuLi-1 epithelium to increasing doses of the isolated Bacillus licheniformis (multiplicity of infection of 10:1, 1:1 or 0.1:1 bacteria: cells) for 1, 3, and 24 h. B. licheniformis and NTHi infection (association and invasion) was assessed using a standard gentamicin survival assay, and epithelial release of IL-6 and IL-8 was measured using a bead based immunoassay.

B. licheniformis was cytotoxic to NuLi-1 cells at 24 h. At 3 h post-challenge, B. licheniformis elicited high IL-6 and IL-8 inflammatory responses from NuLi-1 cells compared with cells treated with heat-treated geogenic dust PM₁₀ (p < 0.0001). Whilst treatment of cells with B. licheniformis increased inflammation, this did not make the cells more susceptible to NTHi infection. This study highlights that geogenic dust PM₁₀ can harbour viable bacterial spores that induce inflammation in respiratory epithelium. The impact on respiratory health from inhalation of bacterial spores in PM₁₀ in arid environments may be underestimated. Further investigation into the contribution of B. licheniformis and the wider dust microbiome to respiratory infection is warranted.

暴露于环境成因（或源自地球）的粉尘可能导致人的呼吸道感染更加频繁和严重。<10 µm（PM ₁₀）的颗粒物是空气污染的组成部分，通常与呼吸道疾病的恶化有关。先前我们已经证明，暴露于地质粉尘PM _10的小鼠经历了对A型流感病毒的炎症反应的加剧。尚不知道地源粉尘PM ₁₀是否还会加剧呼吸道细菌感染，也不知道驱动这些响应的粉尘成分。

我们用来自六个西澳大利亚州偏远城镇的紫外线辐射的成因粉尘PM ₁₀处理了气道支气管上皮细胞（NuLi-1）。观察到高水平的IL-6和IL-8产生，以及持续的微生物生长。生长的16 S rRNA测序确定该微生物为地衣芽孢杆菌（Bacillus licheniformis），一种形成芽孢的环境丰富细菌。接下来，我们在体外调查了地衣芽孢杆菌与呼吸道上皮的相互作用，以确定这是否加剧了细菌性呼吸道病原体（不可分型流感嗜血杆菌，NTHi）的感染。

所有PM ₁₀样品的热处理（100°C）消除了地衣芽孢杆菌污染，并减少了上皮炎症反应，这表明宿主对地质粉尘PM _10的反应中涉及热不稳定和/或微生物因素。然后，我们将NuLi-1上皮暴露于递增剂量的分离的地衣芽孢杆菌中（感染的多重性为10：1、1：1或0.1：1细菌：细胞）1、3和24小时。使用标准的庆大霉素存活测定法评估地衣芽孢杆菌和NTHi感染（关联和侵袭），并使用基于珠的免疫测定法测定IL-6和IL-8的上皮释放。

地衣芽孢杆菌在24 h对NuLi-1细胞具有细胞毒性。攻击后3小时，地衣芽孢杆菌从NuLi-1细胞中诱导出高IL-6和IL-8炎症反应，而经热处理的地源粉尘PM ₁₀处理的细胞则具有这种反应（p  <0.0001）。尽管用地衣芽孢杆菌处理细胞会增加炎症，但这并未使细胞更容易受到NTHi感染。这项研究强调，地源性粉尘PM ₁₀可能带有可存活的细菌孢子，可引起呼吸道上皮发炎。吸入PM ₁₀中细菌孢子对呼吸系统健康的影响在干旱的环境中可能会被低估。有必要进一步研究地衣芽孢杆菌和更广泛的尘埃微生物组对呼吸道感染的贡献。