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Published on: March 18, 2014
Chlamydia trachomatis pneumonia in the severe combined immunodeficiency (SCID) mouse
D M Magee1, J U Igietseme, J G Smith
1Department of Research Immunology, San Antonio State Chest Hospital, TX 78223.
Abstract:
We have developed a model of pneumonia caused by the mouse pneumonitis agent (MoPn, murine Chlamydia trachomatis) in the C.B-17 severe combined immunodeficiency (SCID) mouse. In contrast to our prior models in the nude athymic (nu/nu) and heterozygous (nu/+) mouse, SCID mice lack B-cell function and gamma delta T-cell function. SCID mice were more susceptible to MoPn than nu/nu or nu/+ mice both by criteria of mortality and quantitative lung culture. SCID mice could be reconstituted with thymocytes to be more resistant to MoPn (in the absence of significant antibody production), but the protection was modest and less than that in T-cell reconstituted nu/nu mice in our previous studies. A nu/+ MoPn-specific T-cell clone with a Th1-like cytokine profile also provided modest but significant protection without significant antibody production. The SCID mouse is a useful model to study T-cell-mediated immunity to MoPn in a B cell and gamma delta T-cell-deficient environment.
Insights
Severe combined immunodeficiency (SCID) mice are highly susceptible to mouse pneumonitis agent (MoPn) pneumonia. This model is valuable for studying T-cell immunity in a B-cell deficient environment.
Area of Science:
- Immunology
- Infectious Disease
- Microbiology
Background:
- Murine Chlamydia trachomatis (MoPn) causes pneumonia.
- Previous models used nude athymic (nu/nu) and heterozygous (nu/+) mice.
- Severe combined immunodeficiency (SCID) mice lack B-cell and gamma delta T-cell function.
Purpose of the Study:
- To develop and characterize a pneumonia model using SCID mice.
- To investigate the role of T-cell mediated immunity against MoPn.
- To compare MoPn susceptibility in SCID mice versus other mouse models.
Main Methods:
- Infection of SCID mice with MoPn.
- Assessment of mortality and quantitative lung culture.
- Reconstitution of SCID mice with thymocytes.
- Evaluation of MoPn-specific T-cell clones.
Main Results:
- SCID mice exhibited higher mortality and viral loads compared to nu/nu and nu/+ mice.
- Thymocyte reconstitution conferred modest resistance in SCID mice.
- A Th1-like T-cell clone provided partial protection.
- Antibody production was not a significant factor in protection.
Conclusions:
- SCID mice are a valuable model for studying T-cell immunity to MoPn.
- The model allows investigation in a B-cell and gamma delta T-cell deficient setting.
- T-cell responses play a role in controlling MoPn infection.

