scholarly journals Toll-like receptor signalling induces the expression of serum amyloid A in epidermal keratinocytes and dermal fibroblasts

2018 ◽  
Vol 44 (1) ◽  
pp. 40-46 ◽  
Author(s):  
S. Morizane ◽  
A. Kajita ◽  
K. Mizuno ◽  
T. Takiguchi ◽  
K. Iwatsuki
Keyword(s):  
Serum Amyloid A ◽  
Dermal Fibroblasts ◽  
Serum Amyloid ◽  
Epidermal Keratinocytes ◽  
Toll Like Receptor ◽  
Amyloid A ◽  
Receptor Signalling

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.

scholarly journals Serum Amyloid A Promotes E-Selectin Expression via Toll-Like Receptor 2 in Human Aortic Endothelial Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Eisaku Nishida ◽  
Makoto Aino ◽  
Shu-ichiro Kobayashi ◽  
Kosuke Okada ◽  
Tasuku Ohno ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Toll Like Receptor ◽  
Aortic Endothelial Cells ◽  
Amyloid A ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

Periodontitis is a chronic inflammatory disease that affects the periodontium. Recent studies suggest an association between periodontal and cardiovascular diseases. However, the detailed molecular mechanism is unknown. A previous study has demonstrated that experimental periodontitis induces serum amyloid A (SAA) in the liver and peripheral blood of ApoE-deficient mice as an atherosclerosis model. SAA is an acute-phase protein that affects systemic inflammation. The aim of this study is to investigate the atherosclerosis-onset mechanism using human aortic endothelial cells (HAECs) stimulated by SAAin vitro. Atherosclerosis PCR array and qPCR analyses showed upregulation of adhesion molecules such as intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin in HAECs upon SAA stimulation. In addition, the results demonstrated that Toll-like receptor, TLR2, could serve as an important receptor of SAA in HAECs. Furthermore, small interfering RNA (siRNA) against TLR2 inhibited the upregulation of adhesion molecules in HAECs stimulated by SAA. Our results suggest that SAA stimulates the expression of adhesion molecules via TLR2. SAA could be an important molecule for atherosclerosis induced by periodontal disease.

Serum Amyloid A Aggravates Lipopolysaccharide-Induced Injury of BEAS-2B Cells by Activating Toll-Like Receptor 2/Activator Protein-1 Signaling

2021 ◽  
Vol 11 (2) ◽  
pp. 282-289
Author(s):  
Shiming Yang ◽  
Yumei Qin ◽  
Li Ding ◽  
Jiangbo Wang ◽  
Haiqing Zhao
Keyword(s):  
Cell Viability ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Epithelial Cell Line ◽  
Dependent Manner ◽  
Activator Protein 1 ◽  
Toll Like Receptor ◽  
Concentration Dependent Manner ◽  
Amyloid A ◽  
Activator Protein

The serum amyloid A (sAA) is a common sensitive indicator for the diagnosis of infectious diseases, and sAA levels are increased in pneumonia. However, the detailed molecular mechanism is unknown. Previous studies have demonstrated the participation of Toll-like receptor (TLR) 2 and its downstream protein activator protein-1 (AP-1) in inflammatory lung injury. This study aimed to investigate the effect of sAA on LPS-induced BEAS-2B cells injury and uncover the possible mechanism. The human bronchial epithelial cell line BEAS-2B was exposed to sAA with or without lipopolysaccharide (LPS) treatment, then cell viability, inflammation and apoptosis were evaluated. The effects of TLR2 knockout on sAA + LPS-treated BEAS-2B cells were also determined. Results revealed that sAA treatment reduced cell viability in a concentration-dependent manner and the effect of 500 nM sAA on cell viability was approximately equivalent to LPS. The levels of inflammatory cytokines including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-8, monocyte chemotactic protein (MCP)-1 and IL-6 as well as cell apoptosis and expression of proteins related to apoptosis were significantly increased upon sAA or LPS stimulation. The expression of TLR2 and AP-1 was also elevated in cells challenged with sAA or LPS. Besides, sAA and LPS co-treatment further enhanced the actions of LPS. However, the knockdown of TLR2 obviously blunted the effects of LPS and sAA co-treatment on cell viability, inflammation and apoptosis. Taken together, our results revealed that sAA could exert an enhanced effect on LPS-induced BEAS-2B cells injury via promoting TLR2/AP-1 expression.

Gold nanoparticles induce serum amyloid A 1–Toll-like receptor 2 mediated NF- k B signaling in lung cells in vitro

2018 ◽  
Vol 289 ◽  
pp. 81-89 ◽  
Author(s):  
Cheng Teng Ng ◽  
George Wai Cheong Yip ◽  
Ee Sin Chen ◽  
Wan Yan Rebecca Poh ◽  
Boon Huat Bay ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Lung Cells ◽  
Toll Like Receptor ◽  
Amyloid A ◽  
Toll Like Receptor 2
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