Caballero Ignacio, Mbouamboua Yvon, Weise Susanne, López-Gálvez Raquel, Couralet Marie, Fleurot Isabelle, Pons Nicolas, Barrera-Conde Marta, Quílez-Playán Nayima, Keller Matthieu, Klymiuk Nikolai, Robledo Patricia, Hummel Thomas, Barbry Pascal, Chamero Pablo
Infectiologie et Santé Publique, UMR1282, INRAE, University of Tours, 37380 Nouzilly, France.
Université Côte d'Azur, CNRS, INSERM, Institut de Pharmacologie Moléculaire et Cellulaire, 06560 Sophia Antipolis, France.
Sci Adv. 2025 Feb 28;11(9):eads1568. doi: 10.1126/sciadv.ads1568.
A reduced sense of smell is a common condition in people with cystic fibrosis (CF) that negatively affects their quality of life. While often attributed to nasal mucosa inflammation, the underlying causes of the olfactory loss remain unknown. Here, we characterized gene expression in olfactory epithelium cells from patients with CF using single-nuclei RNA sequencing and found altered expression of olfactory receptors (ORs) and genes related to progenitor cell proliferation. We confirmed these findings in newborn, inflammation-free samples of a CF animal model and further identified ultrastructural alterations in the olfactory epithelium and bulbs of these animals. We established that CFTR, the anion channel whose dysfunction causes CF, is dispensable for odor-evoked signaling in sensory neurons, yet CF animals displayed defective odor-guided behaviors consistent with the morphological and molecular alterations. Our study highlights CF's major role in modulating epithelial structure and OR expression, shedding light on the mechanisms contributing to olfactory loss in CF.
嗅觉减退在囊性纤维化(CF)患者中是一种常见病症,会对他们的生活质量产生负面影响。虽然嗅觉减退通常归因于鼻黏膜炎症,但其潜在病因仍不明。在此,我们使用单核RNA测序对CF患者嗅觉上皮细胞中的基因表达进行了表征,发现嗅觉受体(ORs)及与祖细胞增殖相关的基因表达发生了改变。我们在CF动物模型的新生、无炎症样本中证实了这些发现,并进一步确定了这些动物嗅觉上皮和嗅球的超微结构改变。我们确定,功能障碍导致CF的阴离子通道CFTR在感觉神经元的气味诱发信号传导中并非必需,但CF动物表现出与形态学和分子改变一致的气味引导行为缺陷。我们的研究突出了CF在调节上皮结构和OR表达中的主要作用,为导致CF嗅觉减退的机制提供了线索。