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Infection and Immunity, August 2007, p. 3707-3714, Vol. 75, No. 8
0019-9567/07/$08.00+0     doi:10.1128/IAI.01618-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Survival of Chlamydia muridarum within Dendritic Cells{triangledown}

Jose Rey-Ladino, Xiaozhou Jiang, Brent R. Gabel, Caixia Shen, and Robert C. Brunham*

University of British Columbia Centre for Disease Control, 655 West 12th Avenue, Vancouver, BC V5Z 4R4, Canada

Received 6 October 2006/ Returned for modification 18 December 2006/ Accepted 2 May 2007

Immune responses to Chlamydia trachomatis underlay both immunity and immunopathology. Immunopathology in turn has been attributed to chronic persistent infection with persistence being defined as the presence of organisms in the absence of replication. We hypothesized that dendritic cells (DCs) play a central role in Chlamydia immunity and immunopathology by favoring the long-term survival of C. muridarum. This hypothesis was examined based on (i) direct staining of Chlamydia in infected DCs to evaluate the development of inclusions, (ii) titration of infected DCs on HeLa cells to determine cultivability, and (iii) transfer of Chlamydia-infected DCs to naive mice to evaluate infectivity. The results show that Chlamydia survived within DCs and developed both typical and atypical inclusions that persisted in a subpopulation of DCs for more than 9 days after infection. Since the cultivability of Chlamydia from DCs onto HeLa was lower than that estimated by the number of inclusions in DCs, this suggests that the organisms may be in state of persistence. Intranasal transfer of long-term infected DCs or DCs purified from the lungs of infected mice caused mouse lung infection, suggesting that in addition to persistent forms, infective Chlamydia organisms also developed within chronically infected DCs. Interestingly, after in vitro infection with Chlamydia, most DCs died. However, Chlamydia appeared to survive in a subpopulation of DCs that resisted infection-induced cell death. Surviving DCs efficiently presented Chlamydia antigens to Chlamydia-specific CD4+ T cells, suggesting that the bacteria are able to both direct their own survival and still allow DC antigen-presenting function. Together, these results raise the possibility that Chlamydia-infected DCs may be central to the maintenance of T-cell memory that underlies both immunity and immunopathology.

* Corresponding author. Mailing address: University of British Columbia Centre for Disease Control, 655 West 12th Avenue, Vancouver, BC V5Z 4R4, Canada. Phone: (604) 660-2626. Fax: (604) 660-6066. E-mail: robert.brunham{at}bccdc.ca

{triangledown} Published ahead of print on 14 May 2007.

Editor: J. L. Flynn

Infection and Immunity, August 2007, p. 3707-3714, Vol. 75, No. 8
0019-9567/07/$08.00+0     doi:10.1128/IAI.01618-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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