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Infection and Immunity, December 2001, p. 7419-7424, Vol. 69, No. 12
Department of Pediatric Infectious Diseases,
Arkansas Children's Hospital,1 and
Department of Microbiology and
Immunology,2 University of Arkansas for Medical
Sciences, Little Rock, Arkansas, and Department of Pathology,
Sacred Heart Medical Center, Spokane,
Washington3
Received 10 July 2001/Returned for modification 10 August
2001/Accepted 18 September 2001
Vaginal infection with the mouse pneumonitis agent of
Chlamydia trachomatis (MoPn) produces shorter courses of
infection in C57BL/6 and BALB/c mice than in C3H/HeN mice, while
C57BL/6 mice are more resistant to oviduct pathology. A robust Th1
response is extremely important in host defense against chlamydia. In
this study we examined gamma interferon (IFN-
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.12.7419-7424.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Mouse Strain-Dependent Chemokine Regulation of the
Genital Tract T Helper Cell Type 1 Immune Response
), interleukin 10 (IL-10), and the T-cell-regulatory chemokines macrophage
inflammatory protein-1
(MIP-1
) and monocyte chemoattractant
protein-1 (MCP-1) to determine if differences in these responses
were associated with the differential courses of infection seen in
these three strains of mice. Increased and prolonged IFN-
responses
and lower IL-10 responses were observed in the C57BL/6 strain compared
to BALB/c and C3H. Examination of genital tract chemokines revealed a
marked predominance of MIP-1
over MCP-1 only in the C57 strain.
Thus, a pattern of high MIP-1
and low MCP-1 levels during the first
week of infection is associated with an increased Th1 response and a
shorter, more benign chlamydial infection. Inhibition of the MCP-1
response in C3H mice increased their later T-cell production of IFN-
but decreased their early IFN-
response and had no effect on the course or outcome of infection. Inhibition of MCP-1 is not beneficial in chlamydial infection because of its pleiotropic effects.
*
Corresponding author. Mailing address: Department of
Pediatrics and Microbiology and Immunology, Slot 511, B506C, University of Arkansas for Medical Sciences, Little Rock, AR 72202. Phone: (501)
686-7430. Fax: (501) 320-3551. E-mail:
darvilletonil{at}uams.edu.
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