ClpV1 in avian pathogenic Escherichia coli is a crucial virulence factor contributing to meningitis in a mouse model in vivo.

Meningitis associated with avian pathogenic Escherichia coli (APEC) is an infectious disease of poultry that has gained significant attention because of its potential to infect humans. APEC can utilize two type Ⅵ secretion systems (T6SSs) to efficiently transport toxin effectors into hosts. ClpV1 is one of the core components of the T6SS1. To our knowledge, it has not been clarified how the clpV1 gene contributes to the pathogenicity of meningitis-associated APEC. To investigate the function of the clpV1 gene in the process of Escherichia coli meningitis, a mutant TW-XMΔclpV1 strain was constructed and characterized. In this study, the clpV1 deleted strain displayed a significant decrease in both motility and biofilm formation as well as a reduction in the expression of virulence genes fliC, luxS and ibeA. In vivo studies using mouse and duck models found that the clpV1 deleted groups showed decreased proliferation, fewer lesions and lower expression of inflammatory cytokines in the brain suggesting that clpV1 is involved in the pathogenicity of TWXM. Besides, the decreased quantity of Evans Blue (EB) and the down-regulation of tight junctions (TJs) proteins in the mouse clpV1 deleted group demonstrating a more intact blood-brain barrier (BBB). In conclusion, these results suggest that the clpV1 gene is associated with motility and biofilm formation of TWXM strain and contributes to meningitis by damaging the BBB and brain tissues.