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Essential Roles for Granulocyte-Macrophage Colony-Stimulating Factor
(GM-CSF) and G-CSF in the Sustained Hematopoietic Response of
Listeria monocytogenes-Infected Mice
Yifan Zhan,
Graham J. Lieschke,
Dianne Grail,
Ashley R. Dunn, and
Christina Cheers
From the Department of Microbiology, the University of Melbourne,
Parkville, Victoria, Australia; and the Melbourne Tumour Biology
Branch, Ludwig Institute for Cancer Research, The Royal Melbourne
Hospital, Victoria, Australia.
The in vivo roles of granulocyte-macrophage colony-stimulating
factor (GM-CSF) and granulocyte (G)-CSF were studied in
factor-deficient gene-targeted knockout mice infected with the
facultative intracellular bacterium Listeria monocytogenes.
Previous results showed that G-CSF / mice had an underlying
selective deficiency in granulopoiesis, but GM-CSF/ mice had
little disturbance in resting hematopoiesis. Nevertheless, in this
study it is revealed that 3 days after intraperitoneal infection with 2 × 105 Listeria, GM-CSF/ mice harbored
50-fold more organisms in their spleen and liver than similarly
infected wild-type mice. This was accompanied by a severe depletion of
bone marrow hematopoietic cells and a deficient inflammatory response
in their peritoneal cavity. Thus, GM-CSF is essential for emergency,
but not resting, hematopoiesis. In contrast, G-CSF/ mice were
markedly susceptible to low doses (2 × 104) of
Listeria intraperitoneally. After infection, the acute (1 day)
granulocyte infiltration to the peritoneal cavity was normal compared
with wild type, but the more prolonged monocyte response was deficient,
reflecting a continued decrease in bone marrow cellularity and
hematopoiesis over 3 days, which was not observed in infected wild-type
mice. It is thus apparent that G-CSF deficiency affects monocytopoiesis
as well as granulopoiesis during infection.
Blood, Vol. 91 No. 3 (February 1), 1998:
pp. 863-869
© 1998 by The American Society of Hematology.
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