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Blood, Vol. 95 No. 12 (June 15), 2000:
pp. 3725-3733
"Emergency" granulopoiesis in G-CSF-deficient mice in
response to Candida albicans infection
Sunanda Basu,
George Hodgson,
Hui-Hua Zhang,
Melissa Katz,
Cathy Quilici, and
Ashley R. Dunn
From the Ludwig Institute for Cancer Research, Melbourne Tumor
Biology Branch, PO Royal Melbourne Hospital, Victoria 3050, Australia.
Granulocyte colony-stimulating factor (G-CSF) is a glycoprotein
believed to play an important role in regulating granulopoiesis both at
steady state and during an "emergency" situation. Generation of
G-CSF and G-CSF receptor-deficient mice by gene targeting has demonstrated unequivocally the importance of G-CSF in the regulation of
baseline granulopoiesis. This study attempted to define the physiologic
role of G-CSF during an emergency situation by challenging a cohort of
wild-type and G-CSF-deficient mice with Candida albicans. Interestingly, after infection, G-CSF-deficient mice developed an
absolute neutrophilia that was observed both in blood and bone marrow.
In addition, 3 days after Candida infection increased numbers
of granulocyte-macrophage (GM) and macrophage (M) progenitors were
observed in the bone marrow of G-CSF-deficient mice. Of the cytokines
surveyed, interleukin (IL)-6 levels in serum were elevated; interestingly, levels of IL-6 were higher and more sustained in G-CSF-deficient mice infected with C albicans than similarly
infected wild-type mice. Despite the higher levels of serum IL-6, this cytokine is dispensable for the observed neutrophilia because candida-infected IL-6-deficient mice, or mice simultaneously deficient in G-CSF and IL-6, developed neutrophilia. Similarly, mice lacking both
G-CSF and GM-CSF developed absolute neutrophilia and had elevated
numbers of GM and M progenitors in the bone marrow; thus, G-CSF and
GM-CSF are dispensable for promoting the emergency response to candidal infection.
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