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The Campylobacter jejuni flagellum is a complex, polar proteinaceous appendage that is essential for the bacterium's motility, chemotaxis, and ability to colonize the host gastrointestinal tract (Guerry, 2007). It consists of a basal body, a hook, and a filament composed of two major flagellins, FlaA and FlaB, which are uniquely modified by O-linked glycosylation (Lertsethtakarn et al., 2011). In addition to its role in locomotion, the flagellum acts as a specialized secretion system for virulence factors, such as Campylobacter invasion antigens (Cia), which are necessary for host cell entry and infection (Burnham & Hendrixson, 2018). Because motility is a strict requirement for C. jejuni pathogenesis, the flagellar apparatus is a primary target for the development of anti-virulence agents and vaccines (Hwang et al., 2012). Current therapeutic strategies focus on inhibiting the FlgS/FlgR regulatory system that controls flagellar expression or utilizing flagellin as a vaccine antigen to elicit protective immunity (Neal-McKinney & Konkel, 2012). However, the high degree of phase variation and structural diversity among strains remain significant hurdles for the development of universal treatments (Parkhill et al., 2000).
Inhibition of flagellar assembly via disruption of the FlgS/FlgR two-component system; immune-mediated neutralization of motility; inhibition of flagellar-mediated protein secretion (T3SS).
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