Deficiency of the flagellin subunit FliC exacerbates the pathogenicity of extraintestinal pathogenic Escherichia coli in BALB/c mice by inducing a more intense inflammation.

Extraintestinal pathogenic Escherichia coli (ExPEC) can cause systemic infections in livestock and poultry. Flagellin, a classical virulence factor, acts as a promoter of cell adhesion and invasion, as well as an inducer of inflammatory responses during intestinal pathogen infection. Further understanding is needed regarding the interaction between flagellin and host within the extra-intestinal ecological niche to facilitate a deeper comprehension of ExPEC infection mechanisms. In this study, we constructed a FliC mutant strain (ΔfliC) of ExPEC XM which exhibited reduced motility and enhanced biofilm formation in vitro assays. The ΔfliC strain also demonstrated diminished adherence and invasion capabilities on hBMEC cells while inducing decreased levels of apoptosis. In vivo experiments with BALB/c mice revealed that the ΔfliC strain displayed enhanced pathogenicity compared to wild-type strains, resulting in an earlier time to death, higher tissue load, severe bacteremia, and more intense inflammatory response observed in serum and tissues. These results suggest that the flagellar protein FliC plays different roles for extraintestinal pathogens compared to enteric pathogens. This study further elucidates the functional role of FliC in ExPEC infection while providing a research basis for exploring pathogenic mechanisms and prevention/control strategies for systemic infectious bacterial diseases.