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,
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*
Division of Infectious and Immunological Diseases, British Columbia’s Children’s Hospital,
Canadian Bacterial Diseases Network, and Departments of
Paediatrics,
§
Pathology, and
¶
Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, Canada
The association of Mycobacterium tuberculosis with
alveolar macrophages (M
) in a serum-free environment is a crucial
first step in the pathogenesis of this facultative intracellular
pathogen. We present data demonstrating that freshly explanted alveolar
M do not efficiently bind M. tuberculosis in a
serum-free system, although a small subpopulation of these M
(10–15%) can bind mycobacteria. In contrast, almost 100% of a
peritoneal M population bind mycobacteria under the same conditions.
The poor binding of mycobacteria by alveolar M does not reflect a
general inability to associate with particles; binding and ingestion of
latex beads and zymosan particles were comparable with that seen with
peritoneal M. Resident alveolar M did not efficiently bind
mycobacteria in the presence of serum and expressed poorly several M
surface receptors, including CR3. Furthermore, we demonstrate that
bovine surfactant protein A does not enhance the association of
M. tuberculosis with alveolar M. Differentiation of
alveolar M in vitro resulted in increased expression of M surface
receptors and an increased capacity to bind mycobacteria in the
presence and absence of serum. Evidence is presented that opsonic
binding of M. tuberculosis by differentiated alveolar M
is mediated by complement and CR3, and that the poor binding by
resident alveolar M is due to their poor expression of CR3. The
receptor mediating nonopsonic binding of M. tuberculosis to
differentiated alveolar M was not unequivocally identified in this
study, but could also be CR3.
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