EstA protein, a novel virulence factor of Streptococcus pneumoniae, induces nitric oxide and pro-inflammatory cytokine production in RAW 264.7 macrophages through NF-κB/MAPK

2009 ◽  
Vol 47 (4) ◽  
pp. 196-201 ◽  
Author(s):  
Eun Hee Kang ◽  
Elias Gebru ◽  
Myung Hee Kim ◽  
Henrique Cheng ◽  
Seung-Chun Park
Keyword(s):  
Nitric Oxide ◽  
Streptococcus Pneumoniae ◽  
Virulence Factor ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Protein A ◽  
Raw 264.7 ◽  
Raw 264.7 Macrophages ◽  
Inflammatory Cytokine Production

scholarly journals Inhibitory Effect of N,N-Didesmethylgrossularine-1 on Inflammatory Cytokine Production in Lipopolysaccharide-Stimulated RAW 264.7 Cells

Marine Drugs ◽  
2009 ◽  
Vol 7 (4) ◽  
pp. 589-599 ◽  
Author(s):  
Taiko Oda ◽  
Jong-Soo Lee ◽  
Yuta Sato ◽  
Yasuaki Kabe ◽  
Satoshi Sakamoto ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inhibitory Effect ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Inflammatory Cytokine Production

Nitric Oxide Inhibits Inflammatory Cytokine Production by Human Alveolar Macrophages

1997 ◽  
Vol 17 (3) ◽  
pp. 279-283 ◽  
Author(s):  
Mary Jane Thomassen ◽  
Lisa T. Buhrow ◽  
Mary J. Connors ◽  
F. Takao Kaneko ◽  
Serpil C. Erzurum ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Alveolar Macrophages ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Cytokine Production ◽  
Human Alveolar Macrophages

scholarly journals Persistent Nuclear Factor-κB Activation inUcp2-/- Mice Leads to Enhanced Nitric Oxide and Inflammatory Cytokine Production

2005 ◽  
Vol 280 (19) ◽  
pp. 19062-19069 ◽  
Author(s):  
Yushi Bai ◽  
Hiroki Onuma ◽  
Xu Bai ◽  
Alexander V. Medvedev ◽  
Mary Misukonis ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Inflammatory Cytokine Production

scholarly journals Glycolysis-dependent histone deacetylase 4 degradation regulates inflammatory cytokine production

2014 ◽  
Vol 25 (21) ◽  
pp. 3300-3307 ◽  
Author(s):  
Bin Wang ◽  
Ting-yu Liu ◽  
Chun-Hsiang Lai ◽  
Yan-hua Rao ◽  
Moon-Chang Choi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Response ◽  
Histone Deacetylase ◽  
Inflammatory Cytokine ◽  
Caspase 3 ◽  
Cytokine Production ◽  
Metabolic Reprogramming ◽  
Inflammatory Cytokine Production ◽  
Histone Deacetylase 4 ◽  
Lps Treatment

Activation of the inflammatory response is accompanied by a metabolic shift to aerobic glycolysis. Here we identify histone deacetylase 4 (HDAC4) as a new component of the immunometabolic program. We show that HDAC4 is required for efficient inflammatory cytokine production activated by lipopolysaccharide (LPS). Surprisingly, prolonged LPS treatment leads to HDAC4 degradation. LPS-induced HDAC4 degradation requires active glycolysis controlled by GSK3β and inducible nitric oxide synthase (iNOS). Inhibition of GSK3β or iNOS suppresses nitric oxide (NO) production, glycolysis, and HDAC4 degradation. We present evidence that sustained glycolysis induced by LPS treatment activates caspase-3, which cleaves HDAC4 and triggers its degradation. Of importance, a caspase-3–resistant mutant HDAC4 escapes LPS-induced degradation and prolongs inflammatory cytokine production. Our findings identify the GSK3β-iNOS-NO axis as a critical signaling cascade that couples inflammation to metabolic reprogramming and a glycolysis-driven negative feedback mechanism that limits inflammatory response by triggering HDAC4 degradation.

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