BMC Biol:研究进一步揭示白色念珠菌感染引发机体先天免疫反应的机制

2018-05-04 MedSci MedSci原创

白色念珠菌入侵机体引发机体的先天免疫,通过肌醇1,4,5-三磷酸受体(InsP3R)提高细胞质Ca2 +水平,而这在此过程中起关键作用。然而,连接InsP3R介导的Ca2+增加和免疫反应的分子通路仍尚未清楚。在本研究中,我们发现在巨噬细胞中吞噬白色念珠菌吞噬的过程中,胞外复合物组分2(SEC5)通过结合其C-末端α-螺旋(H1),增加胞质Ca2 +浓度([Ca2 +] c)。免疫荧光显示富集的In

白色念珠菌入侵机体引发机体的先天免疫,通过肌醇1,4,5-三磷酸受体(InsP3R)提高细胞质Ca2 +水平,而这在此过程中起关键作用。然而,连接InsP3R介导的Ca2+增加和免疫反应的分子通路仍尚未清楚。

在本研究中,我们发现在巨噬细胞中吞噬白色念珠菌吞噬的过程中,胞外复合物组分2(SEC5)通过结合其C-末端α-螺旋(H1),增加胞质Ca2 +浓度([Ca2 +] c)。免疫荧光显示富集的InsP3R-SEC5复合物在吞噬体上形成,而重组H1肽导致的InsP3R-SEC5相互作用的破坏减弱了InsP3R介导的Ca2+升高,导致吞噬作用受损。

此外,我们发现白色念珠菌感染促进了InsP3R-SEC5相互作用复合物对Tank-binding kinase 1(TBK1)的募集,从而导致TBK1的活化。随后,活化的TBK1磷酸化干扰素调节因子3(IRF-3)并介导I型干扰素的应答,表明InsP3R-SEC5的相互作用可调节抗真菌先天免疫反应,其方式不仅是通过提高细胞质Ca2 +的水平,还通过激活TBK1-IRF-3通路。

综上所述,该研究结果揭示了InsP3R-SEC5相互作用在针对白色念珠菌的先天免疫反应中的重要作用。

原始出处:

Long Yang, Wenwen Gu, et al., InsP3R-SEC5 interaction on phagosomes modulates innate immunity to Candida albicans by promoting cytosolic Ca2+ elevation and TBK1 activity. BMC Biol. 2018; 16: 46. doi:  10.1186/s12915-018-0507-6

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    2018-05-19 sunylz
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最近,来自匹斯堡大学医学院的研究者们发现了免疫系统抵抗白色念珠菌口腔感染的分子机制。其关键在于白色念珠菌分泌的一类叫做Candidalysin的毒性因子,能够造成口腔内壁细胞层的穿孔,进而激活免疫系统产生防御反应。

J Dent Res:白色念珠菌在牙科丙烯酸表面的早期黏附

义齿相关性口炎是一种常见的念珠菌感染,可能会引起疼痛或其他部位感染源。由于聚(甲基丙烯酸甲酯)(PMMA)仍然是用于制作义齿的主要材料,本研究的目的是通过使用原子力显微镜(AFM)单细胞力光谱学(SCFS)技术来评估白色念珠菌细胞对PMMA表面的粘附作用。

JAMA Ophthalmol:新英格兰静脉吸毒者内源性真菌性眼内炎的暴发

静脉吸毒(IVDA)是内源性真菌性眼内炎的已知风险因子(EFE),其真菌生物体通过静脉而血行传播至眼,导致眼内真菌感染。据报道自2014年以来,随着海洛因相关死亡率的上升,新英格兰的毒品行为猖獗,由毒品引起的真菌性眼内炎的疾病风险也在大幅增加。

J Mycol Med:新型抗菌膜剂可有效对抗白色念珠菌

针对念珠菌感染所形成的生物膜的治疗仍是目前所面临的一大难题。为了克服这个问题,研究人员不断寻找各种来源的新型抗菌膜剂。本研究调查了(1)-N-2-甲氧基苄基-1,10-菲咯啉溴化物(FEN)对白色念珠菌的体外抗菌活性。使用MTT(3-(4-5-二甲基噻唑-2-基)2,5-二苯基四唑鎓溴化物)还原测定确定最小生物膜抑制浓度(MBIC)和最小生物膜减少浓度(MBRC)。使用扫描电子显微镜(SEM)观察

Sci Immunol:机体抵抗口腔疾病的机制

最近,来自匹斯堡大学医学院的研究者们发现了免疫系统抵抗白色念珠菌口腔感染的分子机制。其关键在于白色念珠菌分泌的一类叫做Candidalysin的毒性因子,能够造成口腔内壁细胞层的穿孔,进而激活免疫系统产生防御反应。