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
PubMed

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.