SAA does not induce cytokine production in physiological conditions.
SAA does not induce cytokine production in physiological conditions.
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DOI：
10.1016/j.cyto.2012.10.019
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发表时间：
2013-02
期刊：
影响因子：
3.8
通讯作者：
de Beer, Frederick C.
中科院分区：
文献类型：
--
作者：
Kim, Myung-Hee;de Beer, Maria C.;Wroblewski, Joanne M.;Webb, Nancy R.;de Beer, Frederick C.
SAA has been shown to have potential proinflammatory properties in inflammatory diseases such as atherosclerosis. These include induction of tumor necrosis factor α, interleukin-6, and monocyte chemoattractant protein 1 in vitro. However, concern has been raised that these effects might be due to use of recombinant SAA with low level of endotoxin contaminants or its non-native forms. Therefore, physiological relevance has not been fully elucidated. In this study, we investigated the role of SAA in the production of inflammatory cytokines. Stimulation of mouse monocyte J774 cells with lipid-poor recombinant human SAA and purified SAA derived from cardiac surgery patients, but not ApoA-I and ApoA-II, elicited pro-inflammatory cytokines like granulocyte colony stimulating factor (G-CSF). However, HDL-associated SAA failed to stimulate production of these cytokines. Using neutralizing antibodies against toll like receptor (TLR) 2 and 4, we could evaluate that TLR 2 is responsible for G-CSF production by lipid-poor SAA. To confirm these data in vivo, we expressed mouse SAA in SAA deficient C57BL/6 mice using an adenoviral vector. G-CSF was identically expressed in SAA-Adenoviral infected mice as well as in control null-Adenoviral mice at the early time points (4–8 h) and could not be detected in plasma 24 h after infection when plasma SAA levels were maximally elevated, indicating that adenoviral vector rather than SAA affected G-CSF levels. Taken together, our findings suggest that lipid-poor SAA, but not HDL-associated SAA, stimulates G-CSF production and this stimulation is mediated through TLR 2 in J774 cells. However, its physiological role in vivo remains ambiguous.
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DOI：
10.1161/atvbaha.108.178681
发表时间：
2009-02
期刊：
Arteriosclerosis, thrombosis, and vascular biology
影响因子：
--
作者：
Jahangiri A;de Beer MC;Noffsinger V;Tannock LR;Ramaiah C;Webb NR;van der Westhuyzen DR;de Beer FC
通讯作者：
de Beer FC
血清淀粉样蛋白 A 通过独立于甲酰肽受体-1 的受体介导人中性粒细胞产生活性氧
影响因子：
5.5
作者：
Bjoerkman, Lena;Karlsson, Jennie;Dahlgren, Claes
通讯作者：
Dahlgren, Claes
影响因子：
6
作者：
Mullan, Ronan Hugh;McCormick, Jennifer;Fearon, Ursula
通讯作者：
Fearon, Ursula
影响因子：
6.5
作者：
Sprong, T;Netea, MG;van Deuren, M
通讯作者：
van Deuren, M
影响因子：
4.1
作者：
STRACHAN, AF;SHEPHARD, EG;DEBEER, FC
通讯作者：
DEBEER, FC