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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Activation of the Alternative Complement Pathway by Fungal Melanins
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Activation of the Alternative Complement Pathway by Fungal Melanins

机译：真菌黑色素激活替代补体途径

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Melanins are complex biological pigments formed by the oxidative polymerization of phenolic and/or indolic compounds. These pigments have been implicated in the pathogenesis of some microbial infections, malignancies, degenerative disorders, and autoimmune diseases. Recent studies have demonstrated that melanins have antigenic and anti-inflammatory properties. These findings led us to further explore the interaction of melanins with the immune system. Melanin particles (“ghosts”) were isolated from in vitro-melanized Cryptococcus neoformans cells and Aspergillus niger conidia and then incubated in normal human serum containing 125I-labeled complement C3. The results demonstrated deposition of C3 fragments onto the melanin ghosts as early as 1 min after incubation, with maximum deposition occurring after 12 min for C. neoformans-derived melanin ghosts and after 25 min for A. niger-derived melanin ghosts. The blocking of classical pathway activation did not affect the kinetics or total deposition of C3 onto the melanin ghosts, indicating that melanins activate complement through the alternative pathway. Immunofluorescence analysis of lungs from BALB/c mice injected intratracheally with C. neoformans-derived melanin ghosts demonstrated deposition of C3 fragments onto the ghosts. Small granulomas were also observed surrounding the ghosts. However, melanization of the C. neoformans cell wall did not alter the kinetics or total deposition of C3 fragments onto the fungal cells. The finding that melanin surfaces can activate the complement system suggests a potential mechanism for the pathogenesis of some degenerative and/or autoimmune processes that involve melanized cells as well as another potential role for melanin in the virulence of melanin-producing microorganisms.
机译：黑色素是通过酚类和/或吲哚类化合物的氧化聚合形成的复杂生物颜料。这些色素与某些微生物感染，恶性肿瘤，变性疾病和自身免疫性疾病的发病机理有关。最近的研究表明，黑色素具有抗原和抗炎特性。这些发现使我们进一步探索了黑色素与免疫系统的相互作用。从体外分离的新隐球菌细胞和黑曲霉分生孢子中分离出黑色素颗粒（“幽灵”），然后在含 125 I标记的补体C3。结果表明，最早在孵育后1分钟，C3片段就沉积在黑色素鬼上，而对于 C，最大沉积发生在12分钟后。新甲虫（emeoformans）衍生的黑色素鬼影， A 25分钟后。尼日尔衍生的黑色素鬼魂。经典途径激活的阻断不影响C3在黑色素鬼上的动力学或总沉积，表明黑色素通过替代途径激活补体。气管内注射 C的BALB / c小鼠肺部的免疫荧光分析。源自新福尔摩斯的黑色素鬼影表明C3片段沉积在鬼影上。在幽灵周围还观察到小的肉芽肿。但是， C的变黑了。新福尔摩斯细胞壁未改变C3片段在真菌细胞上的动力学或总沉积。黑色素表面可以激活补体系统的发现暗示了涉及黑色素细胞的一些变性和/或自身免疫过程的发病机理的潜在机制，以及黑色素在产生黑色素的微生物的毒性中的另一潜在作用。

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