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Abstract
Enterhemorrhagic Escherichia coli (EPEC), an important cause of severe infantile diarrheal disease in many parts of the developing world, produced several recently described virulence determinations. Several of its virulence factors are secreted by type III secretion including EspA, which forms filamentous structures on bacterial surface bridging to the host cell’s surface. These structures on bacterial surfaces may deliver other virulence factors directly into the host cell from EHEC. In this study, EspA was expressed in Lactococcus lactis NZ9000 (L. lactis NZ9000). BALB/C mice were immunized by recombinant EspA, and mice sera were assayed for the disruption of E. coli O157:H7 interaction with the host cell. BALB/C mice which were immunized with recombinant EspA produced specific antibody titers, and the difference between the control group and the immune group is marked (P<0.05). The polyclonal mice antisera blocked E. coli O157:H7-induced host cell actin rearrangement and could label E. coli O157:H7 EspA filaments in vitro. Our present findings suggest that L. lactis may be a good candidate to produce oral vaccine, and thus entertains the possibility of developing EspA-oral vaccine in the defense of E. coli O157:H7 infection.
Acknowledgements
We would like to thank the Third Military Medical University for the use of the EspA monoclonal antibody. We also thank Crystal O’Neil for consultation on the manuscript writing and Jing Li for his guidance on the experiment.
Declaration of interest: This research was supported by the National Natural Science Fund Program (20572063) and Shandong Post-Doctoral Innovation Fund Program (200703049). The research was also supported by the State Key Laboratory Of Microbial Techniques And Healthy Clerical Office of Shandong, China. The authors declare no conflicts of interest.