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Infection and Immunity, November 2004, p. 6330-6340, Vol. 72, No. 11
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.11.6330-6340.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

The Infecting Dose of Chlamydia muridarum Modulates the Innate Immune Response and Ascending Infection

Heather K. Maxion, Wei Liu, Mi-Hyang Chang, and Kathleen A. Kelly^*

Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California

Received 7 May 2004/ Returned for modification 9 July 2004/ Accepted 11 August 2004

Murine vaginal infection with the obligate intracellular bacterium Chlamydia muridarum is commonly used as a model for ascending Chlamydia infections of the human female genital tract. Gamma interferon-producing Th1 cells, in concert with other mononuclear infiltrates, primarily mediate antichlamydial immunity. However, many factors modify this response, including the bacterial load. To investigate the manner in which the inoculating dose of C. muridarum modulates a genital infection, we measured innate and adaptive cell numbers, CD4⁺ lymphocyte cytokine profile, chemokine expression, course of infection, and pathological sequelae in genital tracts of BALB/c mice infected with doses of C. muridarum ranging from 10⁴ to 10⁷ inclusion-forming units. We found that the influx of both innate and adaptive immune cells responded similarly in the lower genital tract (cervical-vaginal tissues) and upper genital tract (oviduct tissues) to increasing inoculating doses. However, cells expressing the innate markers Gr-1 and CD11c were affected to a greater degree by increasing dose than lymphocytes of the adaptive immune response (Th1, CD4⁺, CD8⁺, CD19⁺), resulting in a change in the balance of innate and adaptive cell numbers to favor innate cells at higher infecting doses. Surprisingly, we detected greater numbers of viable chlamydiae in the oviducts at lower inoculating doses, and the number of organisms appeared to directly correlate with hydrosalpinx formation after both primary infection and repeat infection. Taken together, these data suggest that innate immune cells contribute to control of ascending infection.

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* Corresponding author. Mailing address: David Geffen School of Medicine at UCLA, Dept. Pathology & Lab. Med., 10833 Le Conte Ave., Mailroom A7-149 CHS, Los Angeles, CA 90095-1732. Phone: (310) 206-5562. Fax: (310) 794-4863. E-mail: kkelly{at}mednet.ucla.edu.

Editor: J. D. Clements

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Infection and Immunity, November 2004, p. 6330-6340, Vol. 72, No. 11
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.11.6330-6340.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

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