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*
Department of Immunology, University of Washington, Seattle, WA 98195; and
Institute for Systems Biology, Seattle, WA 98105
Macrophage activation during the immune response to intracellular
bacteria is critical for resolution of the infection. We have
investigated the pathway of macrophage activation during murine
Mycobacterium bovis bacillus Calmette-Guérin (BCG)
infection. Three distinct phenotypes of macrophages were identified and
compared: resident peritoneal macrophages, day 2 postinfection
macrophages, and 12-day postinfection macrophages. Compared with
resident peritoneal macrophages, day 2 BCG macrophages expressed
intermediate levels of the cell surface receptors Mac1 and F4/80 and
low levels of MHC class II molecules. These cells were highly
phagocytic and produced large amounts of mRNA encoding the chemokine
IP-10. In addition, day 2 BCG macrophages did not generate
reactive nitrogen intermediates, though they were primed to do so, and
did not have increased levels of TNF-
mRNA. Blockade of monocyte
influx into the peritoneal cavity using Abs to platelet endothelial
cell adhesion molecule 1 had no effect on the appearance of day 2 BCG
macrophages, suggesting this cell can differentiate from resident
peritoneal macrophages. In contrast to day 2 BCG macrophages, day 12
BCG macrophages were poorly phagocytic, but produced high levels of
reactive nitrogen intermediates, IP-10 and TNF- mRNA, and class II
MHC molecules. We propose that day 2 BCG macrophages are specialized
for phagocytic uptake of pathogens from the extracellular space,
whereas day 12 BCG macrophages are specialized for killing of the
internalized pathogens. This functional transition during activation is
reminiscent of that seen during maturation/activation of the related
dendritic cell lineage induced by bacterial or inflammatory
stimuli.
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