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<p>Nasal epithelia are amongst the first lines of defense against airway infections. Development of a robust ex vivo nasal epithelia model will enable further mechanistic study of pathogen-upper airway interaction. While the current human nasal epithelia models are limited by their availability and ethical constraints, there is a lack of a robust mouse nasal epithelia model. Here, we developed a functional mouse primary nasal epithelia (MNE) model in an air-liquid interface (ALI). We described an intriguing property of MNE to lose confluence and trans-epithelial electrical resistance (TEER) when initially exposed to ALI conditions, which explains the prior challenges in the development of MNE. Our novel procedure employed two cycles of growth and differentiation to obtain a confluent layer of MNE in ALI. Furthermore, we established MNE as an infectious disease model using <i>Bordetella bronchiseptica</i>, a broad-host spectrum airway pathogen of various animals, including mice. <i>B. bronchiseptica</i> efficiently attached to and colonized the apical face of the MNE, followed by proliferation and disruption of the MNE barrier. Immunostaining indicated that <i>B. bronchiseptica</i> bound cilia of MNE, as they do in vivo in mice. Our results highlight the primary MNE as a powerful tool for studying the interaction between respiratory bacteria and airway epithelia.</p>

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Establishing functional mouse primary nasal epithelia in the air-liquid interface to study bacterial infection

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月31日

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  • Yang Su,
  • Maiya Callender,
  • Maor Bar-Peled,
  • Eric T. Harvill,
  • Thomas Krunkosky

摘要

Nasal epithelia are amongst the first lines of defense against airway infections. Development of a robust ex vivo nasal epithelia model will enable further mechanistic study of pathogen-upper airway interaction. While the current human nasal epithelia models are limited by their availability and ethical constraints, there is a lack of a robust mouse nasal epithelia model. Here, we developed a functional mouse primary nasal epithelia (MNE) model in an air-liquid interface (ALI). We described an intriguing property of MNE to lose confluence and trans-epithelial electrical resistance (TEER) when initially exposed to ALI conditions, which explains the prior challenges in the development of MNE. Our novel procedure employed two cycles of growth and differentiation to obtain a confluent layer of MNE in ALI. Furthermore, we established MNE as an infectious disease model using Bordetella bronchiseptica, a broad-host spectrum airway pathogen of various animals, including mice. B. bronchiseptica efficiently attached to and colonized the apical face of the MNE, followed by proliferation and disruption of the MNE barrier. Immunostaining indicated that B. bronchiseptica bound cilia of MNE, as they do in vivo in mice. Our results highlight the primary MNE as a powerful tool for studying the interaction between respiratory bacteria and airway epithelia.