Gamma interferon levels during Chlamydia trachomatis pneumonia in mice

Area of Science:

• Immunology
• Microbiology
• Infectious Diseases

Background:

• Host defense mechanisms against Chlamydia trachomatis (mouse pneumonitis agent [MoPn]) were examined in a murine model.
• Gamma interferon (IFN-gamma) production in the lungs was observed in both susceptible (nude athymic, nu/nu) and resistant (heterozygous, nu/+) mice during MoPn infection.

Purpose of the Study:

• To investigate the role of gamma interferon (IFN-gamma) in host defense against Chlamydia trachomatis (MoPn) infection.
• To identify the immune cells involved in IFN-gamma production during MoPn infection.

Main Methods:

• In vivo depletion of IFN-gamma in MoPn-infected nude athymic (nu/nu) mice.
• Fluorescence-activated cell sorter (FACS) analysis to identify immune cell populations (GL3 antibody-positive cells, putatively gamma/delta+ T cells).
• In vivo treatment of nu/nu mice with antibodies against NK cells (anti-asialo GM1) or gamma/delta cells (UC7-13D5).
• Treatment of severe combined immunodeficiency (SCID) mice (lacking gamma/delta cells) with anti-NK cell antibody.

Main Results:

• Depletion of IFN-gamma in nu/nu mice led to exacerbated Chlamydia trachomatis infection.
• GL3 antibody-positive cells (putative gamma/delta+ T cells) were induced in the lungs of nu/nu mice during MoPn infection.
• Antibody-mediated depletion of NK cells or gamma/delta cells in nu/nu mice did not significantly reduce lung IFN-gamma levels.
• In SCID mice, NK cell depletion significantly reduced lung IFN-gamma levels.

Conclusions:

• Gamma interferon (IFN-gamma) plays a critical role in controlling Chlamydia trachomatis (MoPn) infection in mice.
• NK cells may contribute to IFN-gamma production in the lungs, particularly in the absence of gamma/delta T cells.