IAI Accepts, published online ahead of print on 19 October 2009

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Infect. Immun. doi:10.1128/IAI.00772-09
Copyright (c) 2009, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Host chemokine and cytokine response in the endocervix within the first developmental cycle of Chlamydia muridarum

Roger G. Rank^*, H. Marie Lacy, Anna Goodwin, James Sikes, Judy Whittimore, Priscilla B. Wyrick, and Uma M. Nagarajan

Departments of Microbiology and Immunology and Pediatrics, University of Arkansas for Medical Sciences and Arkansas Children's Hospital Research Institute, Little Rock, AR; and Department of Microbiology, J.H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN

^* To whom correspondence should be addressed. Email: rankrogerg{at}uams.edu.

The initial host response in a primary chlamydial infection is the onset of acute inflammation. However, we still know very little about the early temporal events in the induction of the acute inflammatory response and how these events relate to the initial chlamydial developmental cycle in an actual genital infection. Because it was critical to initiate a synchronous infection in the endocervix in the first 24 hours to evaluate the sequential expression of the host response, we developed the surgical methodology of depositing C. muridarum directly on the endocervix. Cervical tissue was collected at 3, 12, and 24 hours after inoculation and the expression array of chemokines, cytokines and receptors assessed to characterize the response during the initial developmental cycle. Polymorphonuclear leukocyte (PMN) infiltration was first observed at 12 hours after inoculation and a few PMNs could be seen in the epithelium at 24 hours. Electron microscopic analysis at 24 hours showed that virtually all inclusions were at the same stage of development indicating a synchronous infection. Several chemokine and cytokine genes were expressed as early as 3 hours after infection, but by 12 hours, 41 genes were expressed. Thus, activation of the host response occurs both with the introduction of elementary bodies into the host and early replication of reticulate bodies. No significant response was observed when UV-inactivated organisms were inoculated into the cervix at any time interval. This model provides an ideal opportunity to investigate the mechanisms by which the early inflammatory response is induced in vivo.