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Table 1 GSK3β modulation of the inflammatory response caused by bacterial stimuli

From: Role of glycogen synthase kinase-3 beta in the inflammatory response caused by bacterial pathogens

Bacterium or bacterial PAMP Type of cell GSK3β Inhibition: + pSer9 NF-κB Inhibition ↓ NF-kB Activation ↑ Not tested - Pro or anti- inflammatory molecules Expressed Pro or anti-inflammatory molecules Inhibited Refs.
GSK3β Activation: - pSer9 or + pTyr216
LPS Human monocytes +pSer9 IL-10 IL-1β, IL-6, TNF, IL-12, IFN-α [10, 27]
LPS Human monocytes +pSer9 - IL-1Ra IL-1β [28]
Mycobacterium bovis Primary human monocytes +pSer9 - IL-10 IFN-γ [30]
Muramyl dipeptide Human embryonic kidney epithelial cells +pSer9 - IL-8 [31]
LPS Neonatal mouse cardiac cells   - TNF-α [36]
LPS Mice macrophages + pSer9 - IFNβ - [37]
Burkholderia cenocepacia Human monocytes and mouse macrophages + pSer9 TNF-α, IL-6, IL-8 - [38]
Pam3Cysb and IFN-γ Human macrophages - pSer9 - TNFα IL-10 [39]
Staphylococcus aureus Murine microglia + pTyr216 TNF-α, NO IL10 [40]
LPS Murine microglia A TNF-α - [41]
Salmonella typhimurium Mouse colonic epithelial cells - pSer9; + pTyr216 TNF-α, IL-6 - [33]
IFN-γ and LPS Murine macrophages + pTyr216 - iNOS, NO IL-10 [42]
IFN-γ and LPS Mouse primary microglia and astrocytes A - IL-6, CXCL1, IL-12p40, CCL9, CCL2/MCP-1, P- Selectin,CCL5 CXCL2, MIP2 [43]
  1. A GSK3β phosphorylation at Ser9 or Tyr216 was not analyzed.
  2. b Synthetic PAMP.