美國(guó)和瑞士科學(xué)家近日研究揭示了嗜曙紅細(xì)胞（eosinophil，白細(xì)胞的一種）幫助機(jī)體抵御細(xì)菌感染的機(jī)制,。研究發(fā)現(xiàn)，嗜曙紅細(xì)胞能被細(xì)菌激活，用類似“彈弓”的方式釋放出線粒體DNA,，創(chuàng)建成一張“網(wǎng)”捕獲并殺死細(xì)菌。相關(guān)論文發(fā)表在《自然—醫(yī)學(xué)》（Nature Medicine）上,。
嗜曙紅細(xì)胞僅占人體白細(xì)胞組成的1%-3%,。此前，科學(xué)家已經(jīng)知道它們有助于人體防御寄生蟲(chóng),，但對(duì)于其在免疫系統(tǒng)中的具體角色并不清楚,。與其它種白細(xì)胞遍布全身不同，嗜曙紅細(xì)胞只發(fā)現(xiàn)于消化道等特定區(qū)域,。
之前的研究發(fā)現(xiàn),，在細(xì)菌感染時(shí)，嗜曙紅細(xì)胞會(huì)分泌有毒顆粒蛋白,，這些顆粒蛋白會(huì)殺死細(xì)菌,。在最新的研究中，瑞士伯爾尼大學(xué)的Hans-Uwe Simon和美國(guó)猶他大學(xué)的Gerald J.Gleich及同事發(fā)現(xiàn),，當(dāng)嗜曙紅細(xì)胞受到細(xì)菌感染的刺激時(shí),，它們會(huì)如彈弓發(fā)射一般，快速分泌出線粒體DNA,。線粒體DNA會(huì)綁定在顆粒蛋白上,，形成一張能夠捕獲并殺死細(xì)菌的網(wǎng)。
不過(guò),，嗜曙紅細(xì)胞釋放的有毒蛋白并不總是對(duì)機(jī)體有益,，它也會(huì)損傷附近的組織。比如某些種類的哮喘和克羅恩氏病就要?dú)w因于嗜曙紅細(xì)胞,。
研究人員希望能更多地了解嗜曙紅細(xì)胞“發(fā)射”線粒體DNA的機(jī)制,，他們推測(cè)，這種機(jī)制可能依賴于儲(chǔ)存的能量,，與植物釋放花粉的方式類似,。Gleich說(shuō)：“這是一個(gè)吸引人的發(fā)現(xiàn)，線粒體DNA被發(fā)射出細(xì)胞的時(shí)間要短于1秒,，但我們并不清楚嗜曙紅細(xì)胞怎樣能夠如此快速地彈射出線粒體DNA,。”（生物谷Bioon.com）
生物谷推薦原始出處：
Nature Medicine,，doi:10.1038/nm.1855，Shida Yousefi,，Hans-Uwe Simon
Catapult-like release of mitochondrial DNA by eosinophils contributes to antibacterial defense
Shida Yousefi1, Jeffrey A Gold2, Nicola Andina1, James J Lee3, Ann M Kelly2, Evelyne Kozlowski1, Inès Schmid1, Alex Straumann4, Janine Reichenbach5, Gerald J Gleich6 & Hans-Uwe Simon1
Although eosinophils are considered useful in defense mechanisms against parasites, their exact function in innate immunity remains unclear. The aim of this study is to better understand the role of eosinophils within the gastrointestinal immune system. We show here that lipopolysaccharide from Gram-negative bacteria activates interleukin-5 (IL-5)- or interferon-–primed eosinophils to release mitochondrial DNA in a reactive oxygen species–dependent manner, but independent of eosinophil death. Notably, the process of DNA release occurs rapidly in a catapult-like manner—in less than one second. In the extracellular space, the mitochondrial DNA and the granule proteins form extracellular structures able to bind and kill bacteria both in vitro and under inflammatory conditions in vivo. Moreover, after cecal ligation and puncture, Il5-transgenic but not wild-type mice show intestinal eosinophil infiltration and extracellular DNA deposition in association with protection against microbial sepsis. These data suggest a previously undescribed mechanism of eosinophil-mediated innate immune responses that might be crucial for maintaining the intestinal barrier function after inflammation-associated epithelial cell damage, preventing the host from uncontrolled invasion of bacteria.
