研究显示，血小板可以强化炎症过程

研究显示，血小板可以强化炎症过程

Platelets not only play a key role in blood clotting, but can also significantly intensify inflammatory processes. This is shown by a new study carried out by scientists from the University of Bonn together with colleagues from Sao Paulo (Brazil). In the medium term, the results could open up new ways to treat autoimmune diseases. They have now been published in the renowned journal Cell Reports.

血小板不仅在凝血过程中起关键作用，而且可以显著强化炎症过程。波恩大学的科学家和圣保罗(巴西)的同事进行的一项新的研究表明了这一点。从中期来看，这一结果可能为治疗自身免疫性疾病开辟新的途径。该论文已发表在著名的《细胞报告》杂志上。

For a long time, the role of platelets appeared to be clear: in the event of an injury, they adhere to the wound and stick to each other to rapidly stop the bleeding. This wound closure mechanism works quickly and efficiently, but its protagonists were not considered to have any other functions.

很长一段时间以来，血小板的作用似乎很清楚：一旦受伤，血小板会粘附在伤口上，彼此粘在一起，迅速止血。这种伤口闭合机制工作迅速并有效，但其主角似乎并没有任何其他功能。

For some years now, this picture has begun to change significantly: these tiny cells, each of which is about the size of an intestinal bacterium, are also believed to perform important functions in the immune system. The current study by the universities of Bonn and Sao Paulo supports this thesis: it shows that platelets ensure that the white blood cells (the leukocytes) secrete significantly more inflammatory messengers.

几年来，这种情况已经开始发生重大变化：这些微小的细胞，每一个都有肠道细菌大小，也在免疫系统中发挥着重要作用。波恩大学和圣保罗大学目前的研究支持了这一论点：它表明血小板确保白细胞(白细胞)分泌更多的炎症信使。

In their study, the researchers focused on an important immune mechanism: the activation of the NLRP3 inflammasome. Inflammasomes are molecular machines that consist of a number of different proteins. Among other things, they are able to convert inactive inflammatory messengers into their active form. One of them is the interleukin 1 (IL-1). When cells secrete IL-1, they call on other immune cells to help and thereby trigger a strong inflammatory reaction. As this can also become dangerous for the body, the activity of the inflammasomes, and hence also the formation of IL-1, is strictly regulated.

在他们的研究中，研究人员关注一个重要的免疫机制：NLRP3炎症小体的激活。炎症小体是由许多不同蛋白质组成的分子机器。除此外，它们能够将不活跃的炎症信使转化为活跃的形式。其中之一是白细胞介素1(IL-1)。当细胞分泌IL-1时，它们会召唤其他免疫细胞来帮忙，从而引发强烈的炎症反应。由于这也会对身体造成危险，所以炎症小体的活动，以及IL-1的形成，都受到严格的调控。

As IL-1 promotes inflammation, the messenger substance can significantly worsen the course of autoimmune diseases. Nevertheless, Prof. Franklin is keen to speak up against a one-sided view of platelets as villains: they also intervene in other ways in the immune response, for example by preventing the development of life-threatening sepsis after an infection. Regardless of this, the results might pave the way to new therapies for diseases such as rheumatism or diabetes.

由于IL-1促进炎症反应，其信使物质可显著加重自身免疫性疾病的病程。然而，富兰克林教授强烈反对将血小板视为罪魁祸首的片面观点:它们还会以其他方式干预免疫反应，比如防止感染后出现危及生命的败血症。尽管如此，研究结果可能会为风湿病或糖尿病等疾病的新疗法铺平道路。