Inhibiting F-Actin Polymerization Impairs the Internalization of Moraxella catarrhalis .

Moraxella catarrhalis , a commensal in the human nasopharynx, plays a significant role in the acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Its pathogenicity involves adherence to respiratory epithelial cells, leading to infection through a macropinocytosis-like mechanism. Previous investigations highlighted the diverse abilities of M. catarrhalis isolates with different phenotypes to adhere to and invade respiratory epithelial cells. This study used a murine COPD model and in vitro experiments to explore the factors influencing the pathogenicity of distinct phenotypes of M. catarrhalis . Transcriptome sequencing suggested a potential association between actin cytoskeleton regulation and the infection of lung epithelial cells by M. catarrhalis with different phenotypes. Electron microscopy and Western blot analyses revealed a decrease in filamentous actin (F-actin) expression upon infection with various M. catarrhalis phenotypes. Inhibition of actin polymerization indicated the involvement of F-actin dynamics in M. catarrhalis internalization, distinguishing it from the adhesion process. Notably, hindering F-actin polymerization impaired the internalization of M. catarrhalis . These findings contribute vital theoretical insights for developing preventive strategies and individualized clinical treatments for AECOPD patients infected with M. catarrhalis . The study underscores the importance of understanding the nuanced interactions between M. catarrhalis phenotypes and host lung epithelial cells, offering valuable implications for the management of AECOPD infections.