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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.
Regional Immunology
|November 1, 1993
Summary
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.
