Lester Sarah A, Abdelwahab Sabri H, Randell Scott H, Kelada Samir N P
Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7249, United States.
Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7248, United States.
Toxicol Sci. 2025 Sep 1;207(1):31-36. doi: 10.1093/toxsci/kfaf089.
Exposure to the ambient air pollutant ozone induces acute and chronic respiratory health effects in part by causing inflammation of the airways. Several aspects of the inflammatory response to ozone can be modeled in vitro using primary human bronchial epithelial cells (HBECs) cultured at an air-liquid interface. We tested two commonly used HBEC culture media systems, one proprietary and one non-proprietary, to identify which system yielded the most in vivo-like pro-inflammatory response to acute ozone exposure as reflected by gene expression. Cells from 6 donors were grown in each culture system in parallel, followed by examination of epithelial morphology and cell type proportions prior to ozone exposure. Cultures grown in the proprietary system were notably thicker and contained more ciliated and secretory cells, as well as internal cyst-like structures. The transcriptomic response to acute ozone exposure (0.5 parts per million ozone × 2 h) was strongly affected by media type. HBECs grown in the proprietary system exhibited minimal changes after ozone, with only 7 differentially expressed genes (DEGs). In contrast, HBECs grown in the non-proprietary system exhibited a more dynamic response with 128 DEGs, including hallmark response genes indicative of inflammation (CXCL8) and oxidative stress (HMOX1). Gene set enrichment analysis using the 128 DEGs further corroborated upregulation of oxidative stress and inflammation pathways. In total, our results indicate that the choice of HBEC culture media should be carefully considered to best model the in vivo response to ozone.
暴露于环境空气污染物臭氧会部分通过引发气道炎症而导致急性和慢性呼吸道健康影响。使用在气液界面培养的原代人支气管上皮细胞(HBECs),可以在体外模拟对臭氧炎症反应的几个方面。我们测试了两种常用的HBEC培养基系统,一种是专利产品,一种是非专利产品,以确定哪种系统在基因表达方面对急性臭氧暴露产生最类似体内的促炎反应。来自6名供体的细胞在每个培养系统中平行培养,然后在臭氧暴露前检查上皮形态和细胞类型比例。在专利系统中培养的细胞明显更厚,含有更多的纤毛细胞和分泌细胞,以及内部囊样结构。培养基类型对急性臭氧暴露(百万分之0.5臭氧×2小时)的转录组反应有很大影响。在专利系统中培养的HBECs在臭氧处理后变化最小,只有7个差异表达基因(DEGs)。相比之下,在非专利系统中培养的HBECs表现出更动态的反应,有128个DEGs,包括指示炎症(CXCL8)和氧化应激(HMOX1)的标志性反应基因。使用这128个DEGs进行基因集富集分析进一步证实了氧化应激和炎症途径的上调。总的来说,我们的结果表明,应仔细考虑HBEC培养基的选择,以最好地模拟体内对臭氧的反应。