scholarly journals Serum amyloid A induces interleukin-6 in dermal fibroblasts via Toll-like receptor 2, interleukin-1 receptor-associated kinase 4 and nuclear factor-κB

Immunology ◽  
2014 ◽  
Vol 143 (3) ◽  
pp. 331-340 ◽  
Author(s):  
Steven O'Reilly ◽  
Rachel Cant ◽  
Marzena Ciechomska ◽  
James Finnigan ◽  
Fiona Oakley ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Serum Amyloid A ◽  
Interleukin 1 ◽  
Nuclear Factor Κb ◽  
Dermal Fibroblasts ◽  
Serum Amyloid ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Amyloid A ◽  
Toll Like Receptor 2

scholarly journals Serum Amyloid A Induces Toll-Like Receptor 2-Dependent Inflammatory Cytokine Expression and Atrophy in C2C12 Skeletal Muscle Myotubes

PLoS ONE ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. e0146882 ◽  
Author(s):  
Samantha L. Passey ◽  
Steven Bozinovski ◽  
Ross Vlahos ◽  
Gary P. Anderson ◽  
Michelle J. Hansen
Keyword(s):  
Skeletal Muscle ◽  
Inflammatory Cytokine ◽  
Serum Amyloid A ◽  
Cytokine Expression ◽  
Serum Amyloid ◽  
Toll Like Receptor ◽  
Amyloid A ◽  
Toll Like Receptor 2

scholarly journals Serum amyloid A induces G-CSF expression and neutrophilia via Toll-like receptor 2

Blood ◽  
2009 ◽  
Vol 113 (2) ◽  
pp. 429-437 ◽  
Author(s):  
Rong L. He ◽  
Jian Zhou ◽  
Crystal Z. Hanson ◽  
Jia Chen ◽  
Ni Cheng ◽  
...  
Keyword(s):  
Serum Amyloid A ◽  
Inflammatory Diseases ◽  
Serum Amyloid ◽  
Proteinase K ◽  
In Vivo Studies ◽  
Toll Like Receptor ◽  
Amyloid A ◽  
Toll Like Receptor 2

Abstract The acute-phase protein serum amyloid A (SAA) is commonly considered a marker for inflammatory diseases; however, its precise role in inflammation and infection, which often result in neutrophilia, remains ambiguous. In this study, we demonstrate that SAA is a potent endogenous stimulator of granulocyte colony-stimulated factor (G-CSF), a principal cytokine-regulating granulocytosis. This effect of SAA is dependent on Toll-like receptor 2 (TLR2). Our data demonstrate that, in mouse macrophages, both G-CSF mRNA and protein were significantly increased after SAA stimulation. The induction of G-CSF was blocked by an anti-TLR2 antibody and markedly decreased in the TLR2-deficient macrophages. SAA stimulation results in the activation of nuclear factor–κB and binding activity to the CK-1 element of the G-CSF promoter region. In vitro reconstitution experiments also support that TLR2 mediates SAA-induced G-CSF expression. In addition, SAA-induced secretion of G-CSF was sensitive to heat and proteinase K treatment, yet insensitive to polymyxin B treatment, indicating that the induction is a direct effect of SAA. Finally, our in vivo studies confirmed that SAA treatment results in a significant increase in plasma G-CSF and neutrophilia, whereas these responses are ablated in G-CSF– or TLR2-deficient mice.

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