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Infect. Immun., Dec 1996, 4976-4983, Vol 64, No. 12
KA Kelly, EA Robinson and RG Rank
A Th1-type response develops following vaginal infection with the mouse
pneumonitis biovar of Chlamydia trachomatis (MoPn). Since the type of
response, i.e., Th1 versus Th2, can be influenced by factors present during
T-cell activation, we examined the effects of different routes of MoPn
administration on the cytokine profile and resistance against infection
following a MoPn vaginal challenge. A dominant Th1-type cytokine profile
developed in mice given live MoPn via the intranasal, oral, and vaginal
routes with ratios of gamma interferon-secreting cells to interleukin
4-secreting cells greater than 10. In contrast, mice injected
subcutaneously produced a Th2-type profile with a gamma
interferon/interleukin 4 ratio of only 0.7. These mice also had
significantly higher anti-MoPn immunoglobulin G1 serum titers, confirming a
Th2-type cytokine profile. Exposure of mice to live MoPn, by any route
prior to vaginal challenge, resulted in a shortened course of infection.
However, the subcutaneous group resolved the vaginal infection more slowly,
with 60% (6 of 10 mice) of the mice still isolation positive 12 days after
challenge compared with only 20% of mice given live MoPn by other routes.
Administration of UV-inactivated MoPn did not provide protection against a
vaginal challenge. The decreased ability to clear infection was not
associated with a shift in the cytokine profile, since intranasal and oral
administration of UV- inactivated MoPn resulted in a predominant Th1-type
response. Taken together, these data indicate that the initial route of
MoPn administration can direct the type of response produced after a local
MoPn infection and thus influence the ability of the immune response to
protect against subsequent infection.
Copyright © 1996, American Society for Microbiology
Initial route of antigen administration alters the T-cell cytokine profile produced in response to the mouse pneumonitis biovar of Chlamydia trachomatis following genital infection [published erratum appears in Infect Immun 1997 Jun;65(6):2508]
Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock 72205, USA. kkelly@biomed.uams.edu
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