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Increased phagocytosis of macrophages infected with a ΔrelAΔspoT mutant of enteropathogenic Escherichia coli E2348/69

Increased phagocytosis of macrophages infected with a ΔrelAΔspoT mutant of enteropathogenic Escherichia coli E2348/69

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Journal of Preventive Veterinary Medicine Vol.47, No.3.jpg

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

RESULTS

DISCUSSION

ACKNOWLEDGEMENTS

REFERENCES

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