[观察败血症和自身免疫性疾病与感染和nets形成的关系]。

Akio Matsuhisa, Akira Okui, Yoshiyuki Horiuchi
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引用次数: 2

摘要

中性粒细胞被广泛认为是人体抵御病原体的第一道防线。NETosis于2004年首次被报道为中性粒细胞的程序性细胞死亡,与细胞凋亡和坏死相区别。这一现象已经在基础研究和临床研究中观察到。NETosis由多种刺激物诱导,如PMA、IL-8、DAMPs/PAMPs、细菌和抗原-抗体复合物(包括自身抗体如ANCA)。众所周知,细菌感染后的NETosis有两种类型。虽然它们都有捕获和杀死细菌的能力,但它们也会损害宿主组织。抑制NETs相关酶可阻止NETs在此时形成。由中性粒细胞呼吸爆发产生的O2-触发NETs的形成。在第一类NETosis中,中性粒细胞完全崩溃,而在第二类NETosis中,中性粒细胞保持形态和吞噬能力。然而,细菌可以通过其分泌的核酸酶降解NETs来逃离NETs。因此,使用这些细菌进行感染的动物模型往往会患上严重的传染病。没有Nox2的人慢性肉芽肿病(CGD)患者免疫功能低下,由于NETs形成缺陷,极易感染。另一方面,SLE患者无法分解NETs,因为他们的血清抑制了DNase1活性,这导致了针对NETs和自身dna的自身抗体的产生。感染性疾病、败血症和自身免疫性疾病等炎症性疾病与NETs之间的关系越来越清楚。因此,从NETs的角度重新评估炎症性疾病,并纳入新兴概念以更好地理解所涉及的机制是很重要的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Viewing sepsis and autoimmune disease in relation with infection and NETs-formation].

Neutrophil has been widely recognized as body's first line of defence against pathogens. NETosis was first reported in 2004 as a programmed cell death of neutrophil and distinguished from apoptosis and necrosis. This phenomenon has been already observed in both basic and clinical research. NETosis is induced by various stimulants such as PMA, IL-8, DAMPs/PAMPs, bacteria, and antigen-antibody complex including self-antibody such as ANCA. It is known that there are two types of NETosis following bacterial infections. Although both of them have the ability to capture and kill bacteria, they also damage the host tissues. The inhibition of the NETs-related enzymes prevents the NETs formation at that time. The production of O2- from respiratory burst of neutrophils triggers NETs formation. In the first type of NETosis, neutrophils are completely collapsed, while in the second type, they maintain the morphology and the ability of phagocytosis. However, bacteria can escape from NETs by degrading NETs with their secreting nucleases. Thus the animal models of infection, using these bacteria, oftentimes suffer from severe infectious diseases. Human CGD (Chronic Granulomatosis Disease) patients who do not have Nox2 are immunocompromised, and highly susceptible to infection due to the defect of NETs formation. On the other hand, SLE patients are unable to break down the NETs as their serum inhibits the DNase1 activity, which results in autoantibody generation against NETs as well as self-DNA. It is getting clear that there is a relationship between inflammatory diseases, including infectious diseases, Sepsis and autoimmune diseases, and NETs. Therefore, it is important to re-evaluate the inflammatory disorders from NETs' perspective, and to incorporate the emerging concepts for better understanding the mechanisms involved.

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