Abstract
Escherichia coli is one of the first causes of Gram-negative orthopedic implant infections (OII). Those infections, usually hematogenous, mostly originate from the urinary tract. We investigated the strategies developed by E. coli in this context to evade host innate immune responses, i.e. complement and polymorphonuclear neutrophils (PMN). Twenty strains from OII were compared with 20 strains from bacteremia in patients with non-infected orthopedic implant. In both groups, 6/20 (30 %) strains lysed PMNs, due to the production of the pore-forming toxin α-hemolysin (HlyA). For the others, resistance to phagocytic killing by PMN was not significantly different between both groups. In contrast, resistance to complement-mediated serum killing was significantly higher in OII strains than in the others (65 % vs 10 %; P <0.001). In E. coli, different mechanisms have been involved in complement resistance. Here, serum resistance was not linked to a group 2 capsule, or a loss of outer membrane permeability, or the recruitment of the complement inhibitor C4bp, but was significantly associated with the synthesis of long-chain LPS, regardless of the O-antigen. Thus, serum resistance could promote seeding of peri-implant tissues by helping E. coli to either persist in blood and reach the site of infection or overcome localized complement activation.
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Acknowledgments
We thank Dr J. Holubova and Pr P. Sebo (Laboratory of Molecular Biology of Bacterial Pathogens, Institute of Microbiology of the Academy of Sciences of the Czech Republic, Prague, Czech Republic) for kindly providing the ZKLR+ and Zhly- E. coli control strains used in this study, and Pr S. Bonacorsi (Laboratory of Microbiology, Robert-Debré hospital, AP-HP, Paris, France) for serotyping of a part of the E. coli isolates.
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This work was supported by the French “Ministère de l’Enseignement Supérieur et de la Recherche”.
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Crémet, L., Broquet, A., Jacqueline, C. et al. Innate immune evasion of Escherichia coli clinical strains from orthopedic implant infections. Eur J Clin Microbiol Infect Dis 35, 993–999 (2016). https://doi.org/10.1007/s10096-016-2628-6
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DOI: https://doi.org/10.1007/s10096-016-2628-6