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The Pseudomonas aeruginosa flagellum is a complex, whip-like surface organelle primarily responsible for bacterial motility, including swimming and swarming behaviors [1]. It consists of a basal body, a hook, and a long filament composed of the protein flagellin (FliC), which serves as a critical virulence factor by facilitating chemotaxis and adhesion to host epithelial cells [2]. In addition to its mechanical roles, the flagellum is a potent inducer of the host innate immune response, acting as a ligand for Toll-like receptor 5 (TLR5) and the NLRC4 inflammasome [3]. Therapeutically, the flagellum is a major target for vaccine development and passive immunotherapy, aiming to block bacterial colonization and enhance opsonophagocytic clearance [4]. However, the existence of two distinct serotypes (type a and type b) and the bacterium's ability to downregulate flagellar expression during chronic infection, such as in cystic fibrosis, pose significant challenges for drug development [5].
Inhibition of bacterial motility and adhesion; induction of opsonophagocytic antibodies; activation of TLR5-mediated innate immune responses.
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