Glucocorticoids and Toll-like receptor 2 cooperatively induce acute-phase serum amyloid A

2018 ◽  
Vol 128 ◽  
pp. 145-152 ◽  
Author(s):  
Qi Su ◽  
Günther Weindl
Keyword(s):  
Acute Phase ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Toll Like Receptor ◽  
Amyloid A ◽  
Toll Like Receptor 2 ◽  
Acute Phase Serum

scholarly journals Investigation of the solubility and the potentials for purification of serum amyloid A (SAA) from equine acute phase serum – a pilot study

2013 ◽  
Vol 6 (1) ◽  
Author(s):  
Michelle B Christensen ◽  
Jens Christian Sørensen ◽  
Stine Jacobsen ◽  
Mads Kjelgaard-Hansen
Keyword(s):  
Pilot Study ◽  
Acute Phase ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Acute Phase Serum

In search of the “LINK”: Acute Phase Serum Amyloid A

2011 ◽  
Vol 216 (2) ◽  
pp. 266-268
Author(s):  
Sidika Karakas ◽  
Rami Mortada ◽  
Clinical Fellow
Keyword(s):  
Acute Phase ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Acute Phase Serum

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 Detection of a mediator derived from endotoxin-stimulated macrohpages that induces the acute phase serum amyloid A response in mice.

1979 ◽  
Vol 150 (3) ◽  
pp. 597-606 ◽  
Author(s):  
J D Sipe ◽  
S N Vogel ◽  
J L Ryan ◽  
K P McAdam ◽  
D L Rosenstreich
Keyword(s):  
Acute Phase ◽  
Culture Medium ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Macrophage Response ◽  
Amyloid A ◽  
C3h Mice ◽  
Baseline Values ◽  
Two Stages ◽  
Acute Phase Serum

The mechanism by which LPS stimulates an acute phase serum amyloid A (SAA) response in C3H mice has been studied. A factor (SAA inducer) appears in the blood of C3H/HeN (lipopolysaccharide [LPS]-sensitive) mice approximately 1 h after administration of LPS, which, when passively administered, can induce C3H/HeJ mice to produce SAA although they are resistant to the LPS itself. SAA inducer has been detected in the culture medium of LPS treated C3H/HeN macrophages but not spleen cells. Thus, two stages in the induction of the acute phase SAA response are now recognized: a latent period of 2-3 h during which the SAA concentration remains at baseline values and in which SAA inducer appears, and the period of synthesis of SAA which lasts for approoximately 24 h past induction. It is proposed that a macrophage response to LPS is responsible for production of the serum mediator which induces SAA synthesis.

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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