Bordetella species employ multiple virulence factors to evade host immune responses and establish persistent respiratory infections. Filamentous hemagglutinin (FHA) and adenylate cyclase toxin (ACT) are two key virulence determinants that modulate host immune signaling pathways. Previous studies have shown that FHA contributes to suppression of interleukin-17 (IL-17)-mediated inflammatory responses during infection, yet the molecular mechanisms underlying this immune modulation remain poorly understood. In this study, we investigate the signaling pathways through which FHA suppresses IL-17 production and Th17 immune responses during Bordetella infection. Using macrophage infection models and cytokine profiling, we examine the role of CR3 receptor signaling and downstream transcriptional regulators involved in inflammatory responses. Our findings suggest that FHA-mediated signaling interferes with macrophage activation and IL-23 production, thereby inhibiting Th17 differentiation and IL-17 secretion. Understanding the molecular mechanisms of Bordetella immune evasion provides insights into host–pathogen interactions and may guide the development of improved therapeutic and vaccine strategies.
