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Microbial Immunity and Vaccines

Prior Genital Tract Infection with a Murine or Human Biovar of Chlamydia trachomatis Protects Mice against Heterotypic Challenge Infection

Kyle H. Ramsey, Todd W. Cotter, Rena D. Salyer, Gurwattan S. Miranpuri, Michael A. Yanez, Christoffer E. Poulsen, Jennifer L. DeWolfe, Gerald I. Byrne
Kyle H. Ramsey
Microbiology Department, Chicago College of Osteopathic Medicine, Midwestern University, Downers Grove, Illinois 60515, and
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Todd W. Cotter
Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, Madison, Wisconsin 53706
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Rena D. Salyer
Microbiology Department, Chicago College of Osteopathic Medicine, Midwestern University, Downers Grove, Illinois 60515, and
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Gurwattan S. Miranpuri
Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, Madison, Wisconsin 53706
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Michael A. Yanez
Microbiology Department, Chicago College of Osteopathic Medicine, Midwestern University, Downers Grove, Illinois 60515, and
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Christoffer E. Poulsen
Microbiology Department, Chicago College of Osteopathic Medicine, Midwestern University, Downers Grove, Illinois 60515, and
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Jennifer L. DeWolfe
Microbiology Department, Chicago College of Osteopathic Medicine, Midwestern University, Downers Grove, Illinois 60515, and
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Gerald I. Byrne
Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, Madison, Wisconsin 53706
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DOI: 10.1128/IAI.67.6.3019-3025.1999
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    Fig. 1.

    Primary murine genital tract infection with MoPnC. trachomatis protects against homotypic and heterotypic challenge. The course of infection is shown by solid lines, with each point representing mean IFU from cervical-vaginal swabs of culture-positive mice collected at the time points indicated. Above each point is the ratio of the number of culture-positive animals to the total number of animals in each group. Symbols: ●, previously uninfected controls; ■, mice previously infected with MoPn. (A) Mice challenged with human serovar E (total of two experiments). (B) Mice challenged with human serovar L2 (total of one experiment). (C) Mice challenged with MoPn (total of three experiments).

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    Fig. 2.

    Primary murine genital infection with C. trachomatis serovar E protects against homotypic and heterotypic challenge. The course of infection is shown by solid lines, with each point representing mean IFU from cervical-vaginal swabs of culture-positive mice collected at the time points indicated. Above each point is the ratio of the number of culture-positive animals to the total number of animals in each group. Symbols: ●, previously uninfected controls; ■, mice previously infected with serovar E. (A) Mice challenged with MoPn (total of two experiments). (B) Mice challenged with human serovar L2 (total of one experiment). (C) Mice challenged with serovar E (total of one experiment).

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    Fig. 3.

    Proliferative responses of T lymphocytes to homotypic and heterotypic chlamydial antigens (Ag). Proliferation was assessed by [3H]thymidine incorporation in quadruplicate cultures of nylon wool-enriched T lymphocytes derived from either spleen or ILN in response to UV-inactivated, gradient-purified EBs of C. trachomatis serovar E (closed bars), MoPn (shaded bars), serovar A (open bars), or serovar L2 (hatched bars). (A) Response at day 56 postinfection with serovar E. (B) Response at day 56 postinfection with MoPn. Data are expressed as mean counts per minute above HeLa 229 antigen stimulation for each experimental group (serovar E infected and MoPn infected) and T-cell origin (spleen and ILN). The responses to Hela 229 antigen (and background unstimulated controls) were as follows: ILN (A), 297 ± 91 (176 ± 63); spleen (A), 1,151 ± 217 (927 ± 242); ILN (B), 303 ± 143 (148 ± 54); spleen (B), 2,524 ± 760 (532 ± 158).

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    Fig. 4.

    IgG antibody reactivity at day 56 postinfection with a mouse or human biovar of C. trachomatis. Solubilized gradient-purified EBs of serovar E (lanes A and D) or MoPn (lanes B and C) resolved on 4 to 12% gradient gels and transferred to nitrocellulose were probed with immune plasma collected at day 56 postinfection from a mouse infected with MoPn (lanes C and D) or a mouse infected with serovar E (lanes A and B). Similar results were obtained from a total of eight mice tested (four each MoPn- and serovar E-infected animals). The exposed film was developed and scanned on a Microtek Scanmaker E3 with Photoshop 3.0.5 software. The scanned image was prepared and labeled with QuarkXpress 3.32.

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  • Table 1.

    DTH responses at day 56

    Primary infectionMean (SD) increase in footpad thicknessa in response to:Pb
    MoPn antigenHeLa 229 antigen
    MoPn7.1 (0.5)1.3 (0.5)<0.0001
    Serovar A2.9 (1.8)0.3 (0.4)<0.02
    Serovar E5.3 (1.1)0.2 (0.2)<0.0001
    Serovar L23.6 (1.8)0.2 (0.3)<0.003
    • ↵a Increase in footpad thickness (in millimeters) was measured at 24 h after injection of 5 μg of MoPn antigen and is the mean of 5 mice. Responses in all mice had significantly diminished by 72 h.

    • ↵b By two-tailed t test.

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Prior Genital Tract Infection with a Murine or Human Biovar of Chlamydia trachomatis Protects Mice against Heterotypic Challenge Infection
Kyle H. Ramsey, Todd W. Cotter, Rena D. Salyer, Gurwattan S. Miranpuri, Michael A. Yanez, Christoffer E. Poulsen, Jennifer L. DeWolfe, Gerald I. Byrne
Infection and Immunity Jun 1999, 67 (6) 3019-3025; DOI: 10.1128/IAI.67.6.3019-3025.1999

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Prior Genital Tract Infection with a Murine or Human Biovar of Chlamydia trachomatis Protects Mice against Heterotypic Challenge Infection
Kyle H. Ramsey, Todd W. Cotter, Rena D. Salyer, Gurwattan S. Miranpuri, Michael A. Yanez, Christoffer E. Poulsen, Jennifer L. DeWolfe, Gerald I. Byrne
Infection and Immunity Jun 1999, 67 (6) 3019-3025; DOI: 10.1128/IAI.67.6.3019-3025.1999
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KEYWORDS

Chlamydia Infections
Chlamydia trachomatis
Vaginal Diseases

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