ABSTRACT
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 Mφ that the bacterium enters, is significantly affected by the presence or absence of CR3.
Subject(s)
CD18 Antigens , Macrophage-1 Antigen/genetics , Macrophages/microbiology , Mycobacterium tuberculosis/immunology , Animals , Cell Adhesion , Cell Division , Cell Separation , Cells, Cultured , Hot Temperature , Immunoglobulins , Liver/microbiology , Lung/microbiology , Macrophages, Alveolar/microbiology , Mice , Mice, Knockout , Mycobacterium tuberculosis/growth & development , Opsonin Proteins , Phagocytosis , Spleen/microbiologyABSTRACT
Insertion of a synthetic DNA linker into the repL gene of staphylococcal plasmid pT48 inactivates the replication system. This defect can be complemented in trans by the presence of a pT48 repL gene, but not by the rep genes of the related Staphylococcus areus plasmids pSN2 and pOX1000. Comparison of the sequences of the three replication proteins indicates that specificity may be determined by a putative helix-turn-helix region.
