High-density lipoprotein-associated apolipoprotein A-I: The missing link between infection and chronic inflammation?
High-density lipoprotein-associated apolipoprotein A-I: The missing link between infection and chronic inflammation?
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DOI：
10.1016/s1568-9972(01)00018-0
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发表时间：
2002-02-01
影响因子：
13.6
通讯作者：
Dayer, Jean-Michel
中科院分区：
文献类型：
--
作者：
Burger, Danielle;Dayer, Jean-Michel
包括类风湿关节炎(RA)、多发性硬化症(MS)、系统性红斑狼疮(SLE)和动脉粥样硬化在内的慢性免疫性炎症性疾病的病因还远未阐明。人们普遍认为，这些疾病的发展涉及多种因素，包括遗传易感因素，这些因素以复杂的方式与各种环境因素相互作用，如性别、营养、环境等。此外，感染往往被认为是因果作用。然而，从大量汇编的结果中还没有出现独特的模式，可以为免疫性炎症性疾病的病因提供一个普遍接受的假说，也无法证实或驳斥感染引起持续抗原刺激的可能性。在细胞水平上，慢性炎症的特征是免疫炎症细胞渗入靶组织，这大多发生在组织损伤之前。在炎症部位，单核细胞和T淋巴细胞紧密相连。我们已经证明，受刺激的T淋巴细胞通过接触方式激活单核细胞是一种主要的刺激因素，可以触发大量的肿瘤坏死因子-α(肿瘤坏死因子-α)和白介素1-β(IL-1β)的产生，这在慢性炎症中的重要性是众所周知的。我们最近发现高密度脂蛋白(高密度脂蛋白)相关的载脂蛋白(Apo)A-I是单核巨噬细胞与刺激T细胞接触时产生细胞因子的特异性抑制物。高密度脂蛋白相关的载脂蛋白A-I是一种负性急性期蛋白，即在急性期水平下降超过25%的蛋白。本综述旨在强调高密度脂蛋白相关的载脂蛋白A-I可能起到结构性抗炎因子的作用。急性炎症时血浆高密度脂蛋白相关载脂蛋白A-I水平的降低可能是慢性炎症发展的一个标志，即存在危险因素的个体在感染后可能发展为慢性炎症性疾病。因此，我们假设高密度脂蛋白相关的载脂蛋白A-I可能是感染和慢性炎症之间缺失的一环。
The etiology of chronic immuno-inflammatory diseases including rheumatoid arthritis (RA), multiple sclerosis (MS), systemic lupus erythematosus (SLE), and atherosclerosis is far from being elucidated. It is generally accepted that multiple factors are involved in the development of such pathologies, including factors of genetic susceptibility that interact in complex ways with diverse environmental factors, i.e. gender, nutrition, environment, etc. Furthermore, infection has often been pinpointed as playing a causal role. However, no distinctive pattern has yet emerged from the tremendous number of compiled results that would provide a generally acceptable hypothesis of the etiology of immuno-inflammatory diseases, and the possibility of a persistent antigenic stimulus arising from an infection cannot be confirmed or refuted. At the cellular level, chronic inflammation is characterized by the infiltration of immuno-inflammatory cells into the target tissue, which mostly precedes tissue damage. At the inflammatory site, monocytes and T lymphocytes are in close proximity. We have demonstrated that contact-mediated activation of monocytes by stimulated T lymphocytes is a major stimulus triggering the production of large amounts of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) whose importance in chronic inflammation is well known. We recently established that high-density lipolipoprotein (HDL)-associated apolipoprotein (apo) A-I is a specific inhibitor of cytokine production in monocyte-macrophages upon contact with stimulated T cells. HDL-associated apo A-I is a negative acute-phase protein, i.e. a protein whose level is lowered by more than 25% during the acute phase. This review aims at highlighting the fact that HDL-associated apo A-I might play the role of a constitutive anti-inflammatory factor. The decrease of plasma levels of HDL-associated apo A-I upon acute inflammation may be a sign of the possible development of chronic inflammation, i.e. individuals presenting with risk factors might develop chronic inflammatory diseases after infection. We thus hypothesize that HDL-associated apo A-I might be the missing link between infection and chronic inflammation.