摘要
血清淀粉样蛋白A(SAA)是像C-反应蛋白(CRP)这样的一种急性蛋白,它可作为诊断,预后或治疗许多疾病的跟踪标志。血清SAA的增加是由物理侵袭宿主如感染,创伤,炎症反应和肿瘤导致的。大幅度增加SAA水平的命令变化很大,在严重的细菌感染和慢性炎症性疾病中,从10到100倍再到炎症事件增加到1000倍。产生广泛的响应范围是由于SAA基因复制导致了集群编码SAA的变种以及产生了多种SAA的生物学功能。SAA变异体是简单的结构蛋白和一些翻译后被修饰的单结构域蛋白。SAA1和SAA2诱导炎性细胞因子,而SAA4是变形产生的。我们因此调查,在正常和转化细胞以及它在不同疾病状态下血清水平SAA的表达情况。在低浓度的炎症反应早期(10-100 ng/ml),SAA通过Toll样受体产生chemokines或基质降解酶 ,它还通过G蛋白偶联受体作为一种激动和趋化。当一个感染性或炎性刺激持续存在,肝继续生产更多的SAA(≥ 1000 ng/ml) ,从而通过作为一个直接的细菌调理剂或通过干扰病毒感染与宿主细胞成为抗菌剂。因此,SAA调节先天免疫和适应性免疫,这些信息可以帮助设计更好的药物来治疗特定疾病。
关键词: SAA的变种;FPR2;TLR;
Current Medicinal Chemistry
Title:Structure and Expression of Different Serum Amyloid A (SAA) Variants and their Concentration-Dependent Functions During Host Insults
Volume: 23 Issue: 17
Author(s): Mieke De Buck, Mieke Gouwy, Ji Ming Wang, Jacques Van Snick, Ghislain Opdenakker, Sofie Struyf, Jo Van Damme
Affiliation:
关键词: SAA的变种;FPR2;TLR;
摘要: Serum amyloid A (SAA) is, like C-reactive protein (CRP), an acute phase protein and can be used as a diagnostic, prognostic or therapy follow-up marker for many diseases. Increases in serum levels of SAA are triggered by physical insults to the host, including infection, trauma, inflammatory reactions and cancer. The order of magnitude of increase in SAA levels varies considerably, from a 10- to 100- fold during limited inflammatory events to a 1000-fold increase during severe bacterial infections and acute exacerbations of chronic inflammatory diseases. This broad response range is reflected by SAA gene duplications resulting in a cluster encoding several SAA variants and by multiple biological functions of SAA. SAA variants are single-domain proteins with simple structures and few post-translational modifications. SAA1 and SAA2 are inducible by inflammatory cytokines, whereas SAA4 is constitutively produced. We review here the regulated expression of SAA in normal and transformed cells and compare its serum levels in various disease states. At low concentrations (10-100 ng/ml), early in an inflammatory response, SAA induces chemokines or matrix degrading enzymes via Toll-like receptors and functions as an activator and chemoattractant through a G protein-coupled receptor. When an infectious or inflammatory stimulus persists, the liver continues to produce more SAA (≥ 1000 ng/ml) to become an antimicrobial agent by functioning as a direct opsonin of bacteria or by interference with virus infection of host cells. Thus, SAA regulates innate and adaptive immunity and this information may help to design better drugs to treat specific diseases.
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Cite this article as:
Mieke De Buck, Mieke Gouwy, Ji Ming Wang, Jacques Van Snick, Ghislain Opdenakker, Sofie Struyf, Jo Van Damme , Structure and Expression of Different Serum Amyloid A (SAA) Variants and their Concentration-Dependent Functions During Host Insults, Current Medicinal Chemistry 2016; 23 (17) . https://dx.doi.org/10.2174/0929867323666160418114600
DOI https://dx.doi.org/10.2174/0929867323666160418114600 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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