FMRP, an RNA-binding protein induced by the Mycoplasma pneumonia CARDS toxin, regulates multiciliogenesis and inflammation

作者：Yuling Xu, Tingyu Yang, Shuai Shao, Fengjiao Liu, Nan Song, Jieqiong Li · 发表于：Chinese Medical Journal · 年份：2025 · DOI：10.1097/cm9.0000000000003474 · 被引用次数：1 · 研究领域：RNA modifications and cancer、Pneumonia and Respiratory Infections、RNA and protein synthesis mechanisms

To the Editor: Mycoplasma pneumoniae (M. pneumoniae), an atypical pathogen lacking a cell wall, is a leading cause of community-acquired pneumonia in children; it primarily affects school-age children.[1] The community-acquired respiratory distress syndrome (CARDS) toxin, an adenosine diphosphate-ribosylating and vacuolating exotoxin unique to M. pneumoniae, induces cell swelling and vacuolization.[2] Thus far, the precise functional characteristics of the CARDS toxin have not been fully elucidated. Motile cilia, which extend from specialized epithelial surfaces, perform essential roles during development and disease by facilitating the movement or clearance of fluids and particles through coordinated beating.[3] Fragile X mental retardation protein (FMRP), encoded by the Fmr1 gene, is widely expressed in organs throughout the body. FMRP is enriched in the axonemal central lumen; it has critical roles in multiciliated cell differentiation and multiciliogenesis.[4] A recent report indicated that FMRP is also expressed in the lungs, where it protects the airways from xenobiotic stress.[5] In this study, we investigated whether ciliary FMRP plays a role in the pulmonary immune response during M. pneumoniae infection. All animal experiments were approved by the Capital Medical University Animal Care and Use Committee (No. AEEI-2024-117). BALB/c mice were intratracheally instilled with recombinant CARDS toxin (700 pmol/L) to simulate M. pneumoniae infection, and heat-inactivated C...