Abstract Rationale Respiratory cilia play a crucial role in pulmonary defense by eliminating debris and pathogens through mucociliary clearance. However, several respiratory pathogens exhibit ciliotoxic effects that disrupt the ciliated pseudostratified respiratory epithelium, impairing mucociliary clearance. This study aims to characterize the features of secondary ciliary dyskinesia caused by SARS-CoV-2 (COVID-19), Mycoplasma pneumoniae (M. pneumoniae), and Respiratory Syncytial Virus (RSV). Methods A case-control study was performed on three male patients aged 23, 23, and 38 years who had confirmed infections with SARS-CoV-2, M. pneumoniae, and RSV, respectively. Data from the CILIA4PR Database served as our healthy control. Infections were confirmed via IgM testing. Nasal epithelial brushings were obtained one-week post-infection. High-Speed Video Microscopy Analysis (HSVA) was used to assess ciliary motion and quantify ciliary beat frequency (CBF). Ciliary length was measured using ImageJ. Resulting data was analyzed using the Mann-Whitney U test in GraphPad Prism v10.6.1. Results All three pathogens caused reductions in both ciliary length and CBF. Post-COVID-19 samples exhibited extensive acilia; among the few ciliated cells observed, ciliary length and CBF were significantly reduced versus controls (both p 0.0001). Samples obtained post-M. Pneumoniae infection exhibited apical cell rupture, with a significant reduction in both ciliary length and CBF compared to controls (both p 0.0001). Post-RSV samples showed less pronounced epithelial disruption but demonstrated significantly shortened cilia (p 0.0001) and reduced CBF (p 0.01). Conclusion SARS-CoV-2, Mycoplasma pneumoniae, and RSV impair ciliary function by decreasing beat frequency and shortening ciliary length. Interestingly, each pathogen exhibits a distinct pattern of ciliary damage. SARS-CoV-2 causes marked acilia due to its high ciliotoxicity; M. pneumoniae induces apical cell rupture, damaging epithelial integrity; and RSV causes comparatively mild disruption but significant ciliary shortening. These findings demonstrate the impact of respiratory infections on the upper respiratory ciliated epithelium and the pathogen-specific hallmarks of ciliary damage that contribute to secondary ciliary dyskinesia. This abstract is funded by: Ponce Research Institute
Hernandez-Cordero et al. (Fri,) studied this question.
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