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Infection and Immunity, April 2001, p. 2442-2447, Vol. 69, No. 4
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.4.2442-2447.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Persistent Chlamydia trachomatis Infections Resist Apoptotic Stimuli

Deborah Dean1,2,* and Virginia C. Powers1

Children's Hospital Oakland Research Institute, Oakland, California 94609,1 and Department of Medicine, Division of Infectious Diseases, University of California at San Francisco School of Medicine, San Francisco, California 941102

Received 6 November 2000/Returned for modification 14 December 2000/Accepted 18 January 2001

Microbial modulation of apoptosis has added a new dimension of understanding to the dynamic interaction between the human host and its microbial invaders. Persistent infection can be a by-product of inhibition of apoptosis and may significantly impact the pathogenesis of diseases caused by organisms such as Chlamydia trachomatis. We compared apoptotic responses among HeLa 229 cells acutely and persistently infected and mock infected with serovar A/HAR-13. Persistence was induced by gamma interferon at 0.2 and 2.0 ng/ml. Cells were treated with etoposide or staurosporine at 24-h intervals and assayed for apoptosis by cell count, DNA ladder formation, and cytochrome c translocation. From the 24- to 120-h time points, infected cultures were 87 and 90% viable for etoposide and staurosporine treatment, respectively, and produced no DNA ladder, and cytochrome c remained in the mitochondria. In contrast, mock-infected cells were 22 and 37% viable for etoposide (P = 0.0001) and staurosporine (P = 0.01), respectively, and displayed characteristic DNA ladders, and cytochrome c was translocated. We found that resistance to apoptotic stimuli was identical in acute and persistent infections. Since cytochrome c was not translocated from the mitochondrion, caspase-9 activity was likely not involved. The expression of chlamydial hsp60, a known stimulator of inflammation in vivo, was measured in both active and persistent infections by Western blot, with increased production in the latter with or without staurosporine treatment. Chlamydial disregulation of apoptosis and the ensuing persistence of organisms offer an alternative pathogenic mechanism for chlamydial scarring observed in trachoma and infertility populations via sustained inflammation induced by immunoreactive molecules such as hsp60.

* Corresponding author. Mailing address: Children's Hospital Oakland Research Institute, 5700 Martin Luther King Jr. Way, Oakland, CA 94609. Phone: (510) 450-7655. Fax: (510) 450-7910. E-mail: ddean{at}chori.org.

Infection and Immunity, April 2001, p. 2442-2447, Vol. 69, No. 4
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.4.2442-2447.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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