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B and STAT Signaling Pathways in Human Macrophages1
Department of Virology, National Public Health Institute, Helsinki, Finland
Gram-positive bacteria induce the production of several cytokines
in human leukocytes. The molecular mechanisms involved in Gram-positive
bacteria-induced cytokine production have been poorly characterized. In
this work we demonstrate that both nonpathogenic Lactobacillus
rhamnosus GG and pathogenic Streptococcus
pyogenes (group A streptococci) induce NF-
B and STAT
DNA-binding activity in human primary macrophages as analyzed by EMSA.
NF-B activation was rapid and was not inhibited by a protein
synthesis inhibitor cycloheximide, suggesting that these bacteria could
directly activate NF-B. STAT1, STAT3, and IFN regulatory factor-1
DNA binding was induced by both bacteria with delayed kinetics compared
with NF-B. In addition, streptococci induced the formation of
IFN-
-specific transcription factor complex and IFN-stimulated gene
factor-3 (ISGF3). STAT1 and STAT3 activation and ISGF3 complex
formation were inhibited by cycloheximide or by neutralization with
IFN-/ß-specific Abs. Streptococci were more potent than
lactobacilli in inducing STAT1, ISGF3, and IFN regulatory factor-1 DNA
binding. Accordingly, only streptococci induced IFN- production. The
activation of the IFN- signaling pathway by streptococci could play
a role in the pathogenesis of these bacteria. These results indicate
that extracellular Gram-positive bacteria activate transcription
factors involved in cytokine signaling by two mechanisms: directly,
leading to NF-B activation, and indirectly via cytokines, leading to
STAT activation.
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