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Chlamydial Hsp60-2 Is Iron Responsive in Chlamydia trachomatis Serovar E-Infected Human Endometrial Epithelial Cells In Vitro

Richard W. LaRue,¹ Brian D. Dill,^1* David K. Giles,¹ Judy D. Whittimore,¹ and Jane E. Raulston^1,2,

Departments of Microbiology,¹ Pathology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee²

Received 13 September 2006/ Returned for modification 23 October 2006/ Accepted 10 February 2007

Chlamydial 60-kDa heat shock proteins (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 gamma interferon, result in the development of persistent chlamydial forms that often exhibit enhanced expression of cHsp60. We have shown previously that the expression of cHsp60 is greatly enhanced in Chlamydia trachomatis serovar E propagated in an iron-deficient medium. The objective of this work was to determine which single cHsp60 or combination of the three cHsp60 homologs encoded by this organism responds to iron limitation. Using monospecific polyclonal peptide antisera that recognize only cHsp60-1, cHsp60-2, or cHsp60-3, we found 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.

Published ahead of print on 16 February 2007.

Editor: D. L. Burns

This paper is dedicated to the memory of our friend and colleague, Jane E. Raulston (12 February 2007).