研究顯示，血小板可以強(qiáng)化炎癥過程

研究顯示，血小板可以強(qiáng)化炎癥過程

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.

血小板不僅在凝血過程中起關(guān)鍵作用，而且可以顯著強(qiáng)化炎癥過程。波恩大學(xué)的科學(xué)家和圣保羅(巴西)的同事進(jìn)行的一項(xiàng)新的研究表明了這一點(diǎn)。從中期來看，這一結(jié)果可能為治療自身免疫性疾病開辟新的途徑。該論文已發(fā)表在著名的《細(xì)胞報(bào)告》雜志上。

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.

很長一段時間以來，血小板的作用似乎很清楚：一旦受傷，血小板會粘附在傷口上，彼此粘在一起，迅速止血。這種傷口閉合機(jī)制工作迅速并有效，但其主角似乎并沒有任何其他功能。

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.

幾年來，這種情況已經(jīng)開始發(fā)生重大變化：這些微小的細(xì)胞，每一個都有腸道細(xì)菌大小，也在免疫系統(tǒng)中發(fā)揮著重要作用。波恩大學(xué)和圣保羅大學(xué)目前的研究支持了這一論點(diǎn)：它表明血小板確保白細(xì)胞(白細(xì)胞)分泌更多的炎癥信使。

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.

在他們的研究中，研究人員關(guān)注一個重要的免疫機(jī)制：NLRP3炎癥小體的激活。炎癥小體是由許多不同蛋白質(zhì)組成的分子機(jī)器。除此外，它們能夠?qū)⒉换钴S的炎癥信使轉(zhuǎn)化為活躍的形式。其中之一是白細(xì)胞介素1(IL-1)。當(dāng)細(xì)胞分泌IL-1時，它們會召喚其他免疫細(xì)胞來幫忙，從而引發(fā)強(qiáng)烈的炎癥反應(yīng)。由于這也會對身體造成危險(xiǎn)，所以炎癥小體的活動，以及IL-1的形成，都受到嚴(yán)格的調(diào)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促進(jìn)炎癥反應(yīng)，其信使物質(zhì)可顯著加重自身免疫性疾病的病程。然而，富蘭克林教授強(qiáng)烈反對將血小板視為罪魁禍?zhǔn)椎钠嬗^點(diǎn):它們還會以其他方式干預(yù)免疫反應(yīng)，比如防止感染后出現(xiàn)危及生命的敗血癥。盡管如此，研究結(jié)果可能會為風(fēng)濕病或糖尿病等疾病的新療法鋪平道路。