Abstract

Background: Previous studies have confirmed that ibeA is a key virulence gene of E.coli K1 which plays an important role in the pathogenesis of E.coli K1. The adhesion of E.coli K1 to human brain microvascular endothelial cells is one of the key issues in the pathogenesis of bacterial neonatal meningitis. Biofilm is associated with bacterial adhesion. In this study, the biofilm formation was observed in the IbeA gene deletion mutant, confirming that IbeA is involved in biofilm formation. Methods and materials: The bacteria were divided into four groups: (1) DH5α, (2) E. coli K1, the IbeA knockout strain and the IbeA complemented strain. The biofilm formation was detected by crystal violet staining. The adhesion was measured specifically due to IbeA by comparing the adhesive properties of the IbeA complemented strain to those of the IbeA knockout mutant strain. Results: The formation of biofilm in the wildtype E. coli K1 group was significantly higher than that in the knockout group and in the negative group (p < 0.05). The biofilm formation of the IbeA complemented group was significantly higher than that in IbeA knockout group (p < 0.05). Besides, the adhesion of E. coli K1 was significantly higher than that in the knockout group and the negative group (p < 0.05). The adhesion rate of the IbeA complemented group was significantly higher than that of the IbeA knockout group (p < 0.05). Conclusion: The biofilm formation of E. coli K1 strain is induced by ibeA which is a key virulence gene in the pathogenesis, and ibeA-mediated virulence enhances biofilm-associated adhesion to human brain microvascular endothelial cells in vitro. (Acknowledgements: *Corresponding author: Hong Cao, The study was supported by Undergraduate Training Program for Innovation and Entrepreneurship of SMU, China, No. 201912121275 and Scientific Research Enlightenment Plan of SMU, China,2019)

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