情人節(jié),當(dāng)Bioss遇上Harvard Medical School
發(fā)現(xiàn)你的美麗,熒光標(biāo)記抗體bs-6505R-A647
科研是段跌跌撞撞的旅行,擁有探索未知的美麗——大腦也幫助人體抵御細(xì)菌感染
一直認(rèn)為大腦控制我們的思維意識(shí)和基本的身體機(jī)能,但是近期的一些研究表明,腦神經(jīng)還能調(diào)控機(jī)體對(duì)細(xì)菌感染的防御反應(yīng)。 哈佛醫(yī)學(xué)院的Jesmond Dalli等研究人員進(jìn)一步研究發(fā)現(xiàn):小鼠腹腔的迷走神經(jīng)可分泌神經(jīng)遞質(zhì)乙酰膽堿,調(diào)控淋巴細(xì)胞 ILC3增加 PCTR1的產(chǎn)生和分泌,增強(qiáng)免疫系統(tǒng)的抗菌功能。
感謝你給我的勇氣——PCTR1
PCTR1(protectin conjugate in tissueregeneration 1,組織再生相關(guān)保護(hù)素1)是一類特殊的前炎癥調(diào)節(jié)因子,用于調(diào)控機(jī)體對(duì)炎癥的反應(yīng);它由白細(xì)胞產(chǎn)生其底物為來自魚油的重要脂肪酸——二十二碳六烯酸。
Jesmond Dalli等人發(fā)現(xiàn),切斷小鼠右迷走神經(jīng)會(huì)導(dǎo)致小鼠抵抗大腸桿菌感染的能力嚴(yán)重下降,抗菌能力下降的同時(shí)伴有PCTR1蛋白的顯著降低。此外,還發(fā)現(xiàn)PCTR1的下降會(huì)削弱巨噬細(xì)胞殺死大腸桿菌的能力。
原來你是我最想了解的美麗——小鼠迷走神經(jīng)如何調(diào)控 PCTR1水平
研究發(fā)現(xiàn),迷走神經(jīng)釋放神經(jīng)遞質(zhì)乙酰膽堿促使一種3型天然淋巴細(xì)胞(ILC3)調(diào)控 PCTR1的產(chǎn)生增加;PCTR1反過來也能調(diào)節(jié)巨噬細(xì)胞尋找和殺死細(xì)菌的能力。
Jesmond Dalli等人在切斷迷走神經(jīng)的小鼠體內(nèi)注射PCTR1時(shí),發(fā)現(xiàn) PCTR1能修復(fù)巨噬細(xì)胞的殺菌能力,抑制炎癥反應(yīng),并且促進(jìn)細(xì)菌感染的消退。
原來我們靠得那么近——HARVARD
我們的熒光直標(biāo)一抗 Alexa Fluor-647Anti-15-Lipoxygenase-1,cat#bs-6505R-AF647 被Jesmond Dalli等科研人員用于以上課題研究的流式分析中,其發(fā)表于Cell Immunity期刊(影響因子:24.082)的文章為:“Vagal Regulation of Group 3 Innate LymphoidCells and the Immunoresolvent PCTR1 Controls Infection Resolution”。
應(yīng)用方向:流式分析;樣本:人外周血單核細(xì)胞(PBMCS),小鼠脾。
該研究結(jié)果說明,我們可以利用 PCTR1之類的分子幫助機(jī)體提高自身清除細(xì)菌的能力,而非一味依賴于抗生素。這為今后的抗細(xì)菌感染研究提供了非常大的可能空間。
論文基本信息
【題目】Vagal Regulation of Group 3 Innate LymphoidCells and the Immunoresolvent PCTR1 Controls Infection Resolution
【作者】Jesmond Dalli, Romain A. Colas, HildurArnardottir, Charles N. Serhan,
【期刊】Cell Immunity
【日期】17 Jan 2017
【DOI】http://dx.doi.org/10.1016/j.immuni.2016.12.009
【摘要】Uncovering mechanisms that control immuneresponses in the resolution of bacterial infections is critical for thedevelopment of new therapeutic strategies that resolve infectious inflammationwithout unwanted side effects. We found that disruption of the vagal system inmice delayed resolution of Escherichia coli infection. Dissection of the rightvagus decreased peritoneal group 3 innate lymphoid cell (ILC3) numbers andaltered peritoneal macrophage responses. Vagotomy resulted in an inflammatoryperitoneal lipid mediator profile characterized by reduced concentrations ofpro-resolving mediators, including the protective immunoresolvent PCTR1, alongwith elevated inflammation-initiating eicosanoids. We found that acetylcholineupregulated the PCTR biosynthetic pathway in ILC3s. Administration of PCTR1 orILC3s to vagotomized mice restored tissue resolution tone and host responses toE. coli infections. Together these findings elucidate a host protectivemechanism mediated by ILC3-derived pro-resolving circuit, including PCTR1, thatis controlled by local neuronal output to regulate tissue resolution tone andmyeloid cell responses.
【原文鏈接】http://www.sciencedirect.com/science/article/pii/S1074761316305143