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*
Department of Immunology and Bacteriology, University of Glasgow, Glasgow, United Kingdom; and
Institute for Molecular Biosciences and Department of Biochemistry, University of Queensland, Brisbane, Queensland, Australia
During bacterial infections, the balance between resolution of
infection and development of sepsis is dependent upon the macrophage
response to bacterial products. We show that priming of murine bone
marrow-derived macrophages (BMMs) with CSF-1 differentially regulates
the response to two such stimuli, LPS and immunostimulatory (CpG) DNA.
CSF-1 pretreatment enhanced IL-6, IL-12, and TNF-
production in
response to LPS but suppressed the same response to CpG DNA. CSF-1 also
regulated cytokine gene expression in response to CpG DNA and LPS; CpG
DNA-induced IL-12 p40, IL-12 p35, and TNF- mRNAs were all suppressed
by CSF-1 pretreatment. CSF-1 pretreatment enhanced LPS-induced IL-12
p40 mRNA but not TNF- and IL-12 p35 mRNAs, suggesting that part of
the priming effect is posttranscriptional. CSF-1 pretreatment also
suppressed CpG DNA-induced nuclear translocation of NF-
B and
phosphorylation of the mitogen-activated protein kinases p38 and
extracellular signal-related kinases-1/2 in BMMs, indicating that early
events in CpG DNA signaling were regulated by CSF-1. Expression of
Toll-like receptor (TLR)9, which is necessary for responses to CpG DNA,
was markedly suppressed by CSF-1 in both BMMs and
thioglycolate-elicited peritoneal macrophages. CSF-1 also
down-regulated expression of TLR1, TLR2, and TLR6, but not the LPS
receptor, TLR4, or TLR5. Hence, CSF-1 may regulate host responses to
pathogens through modulation of TLR expression. Furthermore, these
results suggest that CSF-1 and CSF-1R antagonists may enhance the
efficacy of CpG DNA in vivo.
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