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Infection and Immunity, July 2006, p. 3853-3863, Vol. 74, No. 7
0019-9567/06/$08.00+0     doi:10.1128/IAI.02104-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Protein Expression Profiles of Chlamydia pneumoniae in Models of Persistence versus Those of Heat Shock Stress Response

Sanghamitra Mukhopadhyay,1,{dagger} Richard D. Miller,2 Erin D. Sullivan,1 Christina Theodoropoulos,3 Sarah A. Mathews,3 Peter Timms,3 and James T. Summersgill1,2*

Division of Infectious Diseases, Department of Medicine,1 Department of Microbiology and Immunology, University of Louisville School of Medicine, Louisville, Kentucky,2 Infectious Diseases Program, School of Life Sciences, Queensland University of Technology, Brisbane, Australia3

Received 30 December 2005/ Returned for modification 15 February 2006/ Accepted 30 March 2006

Chlamydia pneumoniae is an obligate intracellular pathogen that causes both acute and chronic human disease. Several in vitro models of chlamydial persistence have been established to mimic chlamydial persistence in vivo. We determined the expression patterns of 52 C. pneumoniae proteins, representing nine functional subgroups, from the gamma interferon (IFN-{gamma}) treatment (primarily tryptophan limitation) and iron limitation (IL) models of persistence compared to those following heat shock (HS) at 42°C. Protein expression patterns of C. pneumoniae persistence indicates a strong stress component, as evidenced by the upregulation of proteins involved in protein folding, assembly, and modification. However, it is clearly more than just a stress response. In IFN persistence, but not IL or HS, amino acid and/or nucleotide biosynthesis proteins were found to be significantly upregulated. In contrast, proteins involved in the biosynthesis of cofactors, cellular processes, energy metabolism, transcription, and translation showed an increased in expression in only the IL model of persistence. These data represent the most extensive protein expression study of C. pneumoniae comparing the chlamydial heat shock stress response to two models of persistence and identifying the common and unique protein level responses during persistence.


* Corresponding author. Mailing address: Division of Infectious Diseases, Department of Medicine, Instructional Building, Rm. 311, 500 South Preston St., University of Louisville, Louisville, KY 40292. Phone: (502) 852-5132. Fax: (502) 852-1512. E-mail: j.summersgill{at}louisville.edu.

Editor: J. B. Bliska

{dagger} Present address: Biological Defense Research Directorate, Naval Medical Research Center, 12300 Washington Ave., Rockville, MD 20852.


Infection and Immunity, July 2006, p. 3853-3863, Vol. 74, No. 7
0019-9567/06/$08.00+0     doi:10.1128/IAI.02104-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




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