Proteomic profiles of BpsI-mediated Burkholderia pseudomallei and its roles on antibiotic susceptibility, biofilm formation, stress response and pathogenesis mechanism

Interestingly, Deletion of bpsI genes affected B. pseudomallei's stress response, biofilm formation, antibiotic susceptibility, and pathogenicity in a gene-specific manner. Deletion of bpsI1 or bpsI2 caused reduced heat tolerance, while deletion of bpsI1 or bpsI2 or bpsI3 caused reduced oxidative stress. Deletion of bpsI1 or bpsI3 led to diminished biofilm formation.

For antibiotic susceptibility, deletion of bpsI1, bpsI2 or bpsI3 displayed increased susceptibility to imipenem and ceftazidime. Deletion of bpsI1 or bpsI3 showed increased susceptibility to amoxicillin/clavulonate, while deletion of bpsI2 or bpsI3 was more susceptibility to meropenem. Nevertheless, only deletion of bpsI1 exhibited lower MICs for chloramphenicol.

Moreover, deletion bpsI1 or bpsI2 resulted in decreased pathogenicity during human skin fibroblast infection, associating with weakened virulence in the Galleria mellonella and Caenorhabditis elegans models. However, the deletion of bpsI3 did not affect a virulence in the Galleria mellonella and Caenorhabditis elegans models. Taken together, our findings indicate that the QS system, mediated by BpsI1, BpsI2, and BpsI3, may play a complex and important role in both the environmental adaptation and pathogenicity of B. pseudomallei.