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Mycobacterium tuberculosis infection in complement receptor 3-deficient mice
C Hu1, T Mayadas-Norton, K Tanaka
1Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|August 18, 2000
Summary
Complement receptor type 3 (CR3) is not essential for Mycobacterium tuberculosis infection. Mice lacking CR3 showed similar disease outcomes, indicating alternative pathways for bacterial entry and infection progression.
Area of Science:
- Immunology
- Microbiology
- Pathogenesis
Background:
- Macrophages utilize complement receptor type 3 (CR3) for Mycobacterium tuberculosis (M.tb) phagocytosis.
- CR3 plays a role in host-pathogen interactions during tuberculosis.
Purpose of the Study:
- To investigate the in vivo significance of CR3-mediated phagocytosis in M.tb pathogenesis.
- To determine if CR3 deficiency impacts tuberculosis disease progression.
Main Methods:
- Generated CR3-deficient (CR3-/-) mice on mixed 129SV/C57BL, C57BL/6, and BALB/c backgrounds.
- Infected CR3-/- and wild-type mice with M.tb.
- Assessed survival, bacterial burden, granulomatous lesions, and cytokine expression.
Main Results:
- No significant differences in survival, bacterial burden, or lung/spleen pathology were observed between CR3-/- and wild-type mice.
- Cytokine expression profiles were comparable across groups.
- Absence of CR3 did not alter disease course in resistant (C57BL/6) or susceptible (BALB/c) mouse strains.
Conclusions:
- M.tb can utilize alternative phagocytic receptors for host cell entry in the absence of CR3.
- CR3 is not critical for M.tb pathogenesis or disease progression in mice.
- Host genetic background does not influence the lack of CR3's role in M.tb infection.