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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.