Utilization of CD11b knockout mice to characterize the role of complement receptor 3 (CR3, CD11b/CD18) in the growth of Mycobacterium tuberculosis in macrophages.
Using CD11b knockout mice as a source of macrophages (Mphi;), we show that complement receptor 3 (CR3) mediates approximately 40-50% of nonopsonic binding and 50-60% of serum-mediated binding of Mycobacterium tuberculosis to resident Mphi;. We demonstrate that opsonic binding of M. tuberculosis to Mphi; is mediated by an immunoglobulin-independent, heat-labile component of serum, in both the presence and the absence of CD11b. The survival and replication of M. tuberculosis in an in vitro Mphi; model and an in vivo mouse model of infection were not significantly affected by the absence of CD11b, indicating that CR3-mediated uptake of M. tuberculosis is not a major factor in controlling the subsequent intracellular survival of the mycobacteria. However, whether a mycobacterium will gain access to the intracellular environment, and the type of M&phi; that the bacterium enters, is significantly affected by the presence or absence of CR3.
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Department of Pathology & Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
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Haggar
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Stokes
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D000818:Animals; D018821:CD18 Antigens; D002448:Cell Adhesion; D002455:Cell Division; D002469:Cell Separation; D002478:Cells, Cultured; D006358:Hot Temperature; D007136:Immunoglobulins; D008099:Liver / Q000382:microbiology; D008168:Lung / Q000382:microbiology; D016177:Macrophage-1 Antigen / Q000235:genetics*; D008264:Macrophages / Q000382:microbiology*; D016676:Macrophages, Alveolar / Q000382:microbiology; D051379:Mice; D018345:Mice, Knockout; D009169:Mycobacterium tuberculosis / Q000254:growth & development / Q000276:immunology*; D009895:Opsonin Proteins; D010587:Phagocytosis; D013154:Spleen / Q000382:microbiology
D018821:CD18 Antigens; D007136:Immunoglobulins; D016177:Macrophage-1 Antigen; D009895:Opsonin Proteins