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J. Bacteriol. doi:10.1128/JB.01037-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Polyphosphate kinase 1 (PPK1) is a pathogenesis determinant in Campylobacter jejuni

University of British Columbia, Department of Microbiology and Immunology, Vancouver, BC, Canada; Vaccine and Infectious Disease Organization, Saskatoon, SK, Canada; Stanford University, Department of Biochemistry, Stanford, CA, USA

^* To whom correspondence should be addressed. Email: egaynor{at}interchange.ubc.ca.

	Abstract

Campylobacter jejuni is the leading cause of bacterial gastroenteritis in the developed world. Despite its prevalence, relatively little is known about C. jejuni's precise pathogenesis mechanisms, particularly in comparison to other well-studied enteric organisms like E. coli and Salmonella spp. Altered expression of phosphate genes in a C. jejuni stringent response mutant, together with known correlations between the stringent response, polyphosphate (poly P), and virulence in other bacteria, led us to investigate the role of poly P in C. jejuni stress survival and pathogenesis. All sequenced C. jejuni strains harbour a conserved putative PPK1 predicted to be principally responsible for poly P synthesis. We generated a targeted ppk1 deletion mutant (ppk1) in C. jejuni strain 81-176 and found that ppk1, as well as the spoT stringent response mutant, exhibited low levels of poly P at all growth stages. In contrast, wild-type C. jejuni poly P levels increased significantly as the bacteria transitioned from log to stationary phase. Phenotypic analyses revealed that the ppk1 mutant was defective for survival during osmotic shock and low-nutrient stress. However, certain phenotypes associated with ppk1 deletion in other bacteria (i.e., motility, oxidative stress) were unaffected in the C. jejuni ppk1 mutant, which also displayed an unexpected increase in biofilm formation. The C. jejuni ppk1 mutant was also defective for the virulence–associated phenotype of intra-epithelial cell survival in a tissue culture infection model and exhibited a striking, dose-dependent chick colonization defect. These results indicate that poly P utilization and accumulation contribute significantly to C. jejuni pathogenesis and affect its ability to adapt to specific stresses and stringencies. Furthermore, our study demonstrates that poly P likely plays both similar and unique roles in C. jejuni compared to other bacteria, and that poly P metabolism is linked with stringent response mechanisms in C. jejuni.

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