Adenosine Triphosphate Released by Candida albicans Is Associated with Reduced Skin Infectivity.
Adenosine Triphosphate Released by Candida albicans Is Associated with Reduced Skin Infectivity.
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白色念珠菌释放的三磷酸腺苷与皮肤感染性降低有关。
DOI：
10.1016/j.jid.2021.03.010
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Kaplan,DanielH
中科院分区：
文献类型：
--
作者：
Zhang,Shiqun;Edwards,TaraN;Mogavero,Selene;Mathers,AliciaR;Hube,Bernhard;Berman,Judith;Bougnoux,Marie-Elisabeth;D'Enfert,Christophe;Kaplan,DanielH
皮肤是暴露于肠道微生物和病原体的屏障组织。白色念珠菌是一种二型真菌，通常在屏障表面共生生长，但也可能具有致病性（Gow等人，2011年）。致病性皮肤梭菌白色念珠菌感染诱导提供宿主防御的17型免疫（Kashem和Kaplan，2016）。C.白色念珠菌皮肤感染由病原体衍生的Toll样受体和Dectin-1配体的识别触发（Netea等，2008年）。近年来，E.已经显示肠中的大肠杆菌和一些其它细菌物种调节适应性肠反应的发展（Atarashi等人，2008; Proietti等人，2019年）。酵母酿酒酵母也主动释放eATP（Peters等人，2015年）。为了确定C.白念珠菌释放eATP以及这是否会影响宿主的免疫应答，我们首先检测了PBS洗涤的对数中期C.在30 ℃下孵育或在100 ℃下热灭活1小时的白色念珠菌SC 5314酵母。活C.白色念珠菌显示显著量的eATP，其接近通过热杀死获得的水平（图1a）。在酵母提取物蛋白胨葡萄糖培养基（1%酵母提取物、2%蛋白胨、2%葡萄糖）中生长的SC 5314酵母的动力学分析显示，肉汤中的eATP在对数中期达到峰值6小时。碘化丙啶染色流式细胞仪分析细胞活力显示< 0.5% staining at all the time points tested compared with>99%的碘化丙啶对热灭活的C.白色念珠菌（图1a和补充图S1 a）。接下来，我们比较了常见原养型SC 5314衍生的实验室菌株的生长动力学和eATP分泌。值得注意的是，SC 5314和CAI 4释放eATP，而RM 1000、SN 87 HL和BWP 17几乎不释放eATP（图1c和d）。用CAI 4和RM 1000（具有相似生长动力学的两种遗传相关菌株）进行的表皮感染揭示了分泌更多eATP的CAI 4导致比RM 1000更低的集落形成单位（CFU）（图1 e）（Igyártó等人，2011; Kashem等人，2015年）的报告。这些数据表明，与细胞死亡无关的eATP释放在普通实验室C中是可变的。白念珠菌菌株，并可能增加皮肤宿主防御，虽然CAI 4和RM 1000之间的遗传差异也可能解释这些结果。
Skin is a barrier tissue that is exposed to both commensal microorganisms and pathogens. Candida albicans is a dimorphic fungus that typically grows as a commensal at barrier surfaces but can also become pathogenic (Gow et al., 2011). Pathogenic cutaneous C. albicans infection induces type-17 immunity that provides host defense (Kashem and Kaplan, 2016). The innate response of C. albicans skin infections is triggered by the recognition of the pathogen-derived toll-like receptor and Dectin-1 ligands (Netea et al., 2008). Recently, extracellular adenosine triphosphate (eATP) released by E. coli in the intestine and some other bacteria species have been shown to modulate the development of adaptive intestinal responses (Atarashi et al., 2008; Proietti et al., 2019). The yeast Saccharomyces cerevisiae also actively releases eATP (Peters et al., 2015). To determine whether C. albicans releases eATP and whether this can affect the host immune response, we first examined the eATP released from PBS-washed mid-logarithm-phase C. albicans SC5314 yeast that were incubated at 30 C or heat-killed at 100 C for 1 hour. The quantity of eATP in the centrifuged supernatant of live C. albicans showed a significant amount of eATP that approached the level obtained by heat killing (Figure 1 a). A kinetic analysis of SC5314 yeast grown in yeast extract peptone dextrose media (1% yeast extract, 2% peptone, 2% dextrose) revealed eATP in the broth, which peaked 6 hours during the mid-logarithm phase. Flow cytometry analysis with propidium iodide staining for cell viability showed< 0.5% staining at all the time points tested compared with> 99% propidium iodide positivity for heat-killed C. albican (Figure 1 a and Supplementary Figure S1 a). We next compared the growth kinetics and the eATP secretion in a collection of common prototrophic SC5314-derived laboratory strains. Notably, SC5314 and CAI4 released eATP, whereas RM1000, SN87HL, and BWP17 released little eATP (Figure 1 c and d). Epicutaneous infection with CAI4 and RM1000, two genetically related strains with similar growth kinetics, revealed that CAI4, which secreted more eATP, resulted in lower colony-forming units (CFUs) than RM1000 (Figure 1 e)(Igyártó et al., 2011; Kashem et al., 2015). These data suggest that the eATP released unrelated to cell death is variable within common laboratory C. albicans strains and may augment cutaneous host defense, although genetic differences between CAI4 and RM1000 could also potentially explain these results.
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