Effects ofibeADeletion on Virulence and Biofilm Formation of Avian PathogenicEscherichia coli
ABSTRACTTheibeAgene is located on a genomic island, GimA, which is involved in the pathogenesis of neonatal meningitisEscherichia coli(NMEC) and avian pathogenicE. coli(APEC). The prevalence ofibeAin the APEC collection in China was investigated, and 20 of 467 strains (4.3%) were positive. In addition, analysis of the association of theE. colireference (ECOR) groups with positive strains revealed thatibeAwas linked to group B2. TheibeAgene in DE205B was analyzed and compared to those of APEC and NMEC, which indicated that the specificity ofibeAwas not consistent along pathotypes. The invasion of chicken embryo fibroblast DF-1 cells by APEC DE205B and RS218 was observed, which suggested that DF-1 cells could be a model to study the mechanism of APEC invasion. The inactivation ofibeAin APEC DE205B led to the reduced capacity to invade DF-1 cells, defective virulencein vivo, and decreased biofilm formation compared to the wild-type strain. In addition, strain AAEC189 expressingibeAexhibited enhanced invasion capacity and biofilm formation. The results of the quantitative real-time reverse transcription-PCR (qRT-PCR) analysis and animal system infection experiments indicated that the loss ofibeAdecreased the colonization and proliferation capacities of APEC in the brain during system infection.