Mycobacterium avium Infection in a C3HeB/FeJ Mouse Model

Area of Science:

• Immunology
• Infectious Diseases
• Animal Models

Background:

• Mycobacterium avium complex (MAC) infections are a growing global health concern, particularly MAC lung disease.
• Current treatments for MAC lung disease are prolonged, poorly tolerated, and often ineffective.
• There is a critical need for better animal models to study MAC pathogenesis and test new therapies.

Purpose of the Study:

• To evaluate the C3HeB/FeJ mouse model for its ability to replicate human MAC lung disease.
• To assess the development of pulmonary pathology and immune responses in C3HeB/FeJ mice infected with MAC.

Main Methods:

• C3HeB/FeJ mice were infected with a rough strain of MAC 2285 via aerosol.
• Lung bacterial burden, granuloma formation, necrosis, and immune cell infiltration (CD4+ Th1, Th17, Treg) were monitored over time.

Main Results:

• Mice developed a progressive lung infection with increasing bacterial burden peaking around day 40.
• Granulomas showed micronecrosis and infiltration of CD4+ Th1, Th17, and Treg lymphocytes.
• During chronic infection (day 50+), bacterial burden plateaued with reduced Th1/Th17 cells and increased Treg cells and necrosis.

Conclusions:

• The C3HeB/FeJ mouse model successfully recapitulates key features of human MAC lung disease, including progressive infection, granuloma necrosis, and specific immune cell dynamics.
• This model is valuable for investigating the immune pathogenesis of nontuberculous mycobacteria (NTM) and for screening novel therapeutic compounds.