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Infect. Immun. doi:10.1128/IAI.01465-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Chlamydial Hsp60-2 is iron-responsive in Chlamydia trachomatis serovar E-infected human endometrial epithelial cells in vitro

Departments of Microbiology and Pathology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee

^* To whom correspondence should be addressed. Email: raulston{at}mail.etsu.edu.

	Abstract

Chlamydial heat shock proteins 60kDa (cHsp60s) are known to play a prominent role in the immunopathogenesis of disease. It is also known that several stress-inducing growth conditions, such as heat, iron deprivation, or exposure to interferon gamma (IFN-), result in the development of persistent chlamydial forms that often show enhanced expression of cHsp60. We have shown that the expression of cHsp60 is greatly enhanced in Chlamydia trachomatis serovar E propagated in an iron-deficient medium. The objective of this work is to determine which one, or combination, of three cHsp60 homologs encoded by this isolate responds to iron limitation. Using monospecific, polyclonal peptide antisera, that exclusively recognize cHsp60-1, cHsp60-2 and cHsp60-3, we show that expression of cHsp60-2 is responsive to iron deprivation. Overall, our studies suggest that the expression of cHsp60 homologs differs among the mechanisms currently known to induce persistence.