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Infection and Immunity, June 2007, p. 2776-2785, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.01095-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Extraintestinal Pathogenic Escherichia coli Survives within Neutrophils{triangledown}

Helen Nazareth,1,2,3 Stacy A. Genagon,1,3 and Thomas A. Russo1,2,3,4*

Department of Medicine,1 Department of Microbiology,2 The Witebsky Center for Microbial Pathogenesis,3 Veterans Administration Western New York Healthcare System, University at Buffalo, Buffalo, New York4

Received 13 July 2006/ Returned for modification 23 August 2006/ Accepted 30 January 2007

Extracellular pathogenic Escherichia coli (ExPEC) strains are common causes of a variety of clinical syndromes, including urinary tract infections, abdominal infections, nosocomial pneumonia, neonatal meningitis, and sepsis. ExPEC strains are extracellular bacterial pathogens; therefore, the innate immune response (e.g., professional phagocytes) plays a crucial role in the host defense against them. Studies using the model ExPEC strain CP9 demonstrated that it is relatively resistant to neutrophil-mediated bactericidal activity. Although this could be due to resistance to phagocytosis, the ability of CP9 to survive the intracellular killing mechanisms of neutrophils is another possibility. Using a variation of the intracellular invasion assay, we studied the survival of CP9 within peripheral blood-derived human neutrophils. Our results indicated that CP9 did survive within human neutrophils, but we were unable to demonstrate that intracellular replication occurred. This finding was not unique to CP9, since when a conservative assessment of survival was used, four of six additional ExPEC strains, but not an E. coli laboratory strain, were also capable of survival within neutrophils. Initial studies in which we began to decipher the mechanisms by which CP9 is able to successfully survive intracellular neutrophil-mediated bactericidal activity demonstrated that CP9 was at least partially susceptible to the neutrophil oxidative burst. Therefore, absolute resistance to the oxidative burst is not a mechanism by which ExPEC survives within neutrophils. In addition, electron microscopy studies showed that CP9 appeared to be present in phagosomes within neutrophils. Therefore, avoidance of phagosomal uptake or subsequent escape from the phagosome does not appear to be a mechanism that contributes to CP9's survival. These findings suggest that survival of ExPEC within neutrophils may be an important virulence mechanism.

* Corresponding author. Mailing address: Department of Medicine, Division of Infectious Diseases, 3435 Main St., Biomedical Research Building, Room 141, Buffalo, NY 14214. Phone: (716) 829-2674. Fax: (716) 829-3889. E-mail: trusso{at}acsu.buffalo.edu

{triangledown} Published ahead of print on 12 February 2007.

Editor: J. B. Bliska

Infection and Immunity, June 2007, p. 2776-2785, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.01095-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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