Enteropathogenic Escherichia coli (EPEC) have developed survival strategies to evade host defense systems. The intracellular level of guanosine tetraphosphate (ppGpp) controlled by RelA and SpoT can mediate immune evasion of EPEC. However, the impact of ppGpp-defective EPEC infection on phagocytes remains unknown. In this study, we report that disrupting relA and spoT of EPEC E2348/69 strain promotes its phagocytosis in porcine macrophages. Our experimental analysis showed that both uptake and killing of an E2348/69 ΔrelAΔspoT mutant by macrophages were increased compared to those of wildtype strain. These results suggest that ppGpp plays an essential role in evading phagocytosis during EPEC pathogenesis.

INTRODUCTION
MATERIALS AND METHODS
    Bacterial strains and plasmids used in this study
    Determination of minimum bactericidal concentrationsfor gentamicin
    Gentamicin protection assay
    Statistical analysis
RESULTS
    Infection by ΔrelAΔspoT EPEC promotes bacterialuptake of 3D4/31 cells
    Bacterial killing is enhanced in 3D4/31 cells infectedwith ΔrelAΔspoT EPEC
DISCUSSION
ACKNOWLEDGEMENTS

• Jang Won Yoon(College of Veterinary Medicine & Institute of Veterinary Science, Kangwon National University, Chuncheon, Gangwon 24341, Korea) Corresponding Author
• Jun Bong Lee(College of Veterinary Medicine & Institute of Veterinary Science, Kangwon National University, Chuncheon, Gangwon 24341, Korea)