Regulation of Candida albicans morphogenesis by fatty acid metabolites
Regulation of Candida albicans morphogenesis by fatty acid metabolites
复制标题
DOI：
10.1128/iai.72.11.6206-6210.2004
复制
发表时间：
2004-11-01
影响因子：
3.1
通讯作者：
Huffnagle, GB
中科院分区：
文献类型：
--
作者：
Noverr, MC;Huffnagle, GB
白色念珠菌是一种机会性二型真菌，栖息于各种宿主粘膜部位。从酵母到菌丝形式的转化与增加的毒力和粘膜侵袭性有关。C.白念珠菌的形态发生受多种信号和信号通路的调控。然而，在体内控制形态发生的信号是未知的。我们研究了宿主长链脂肪酸、类花生酸和细菌短链脂肪酸对发芽控制的影响。测试的C-18或C-20脂肪酸（花生四烯酸、油酸、亚麻酸或γ-亚麻酸）均对增强芽管形成没有作用。在不同类花生酸中，前列腺素E-2和血栓素B-2均显著促进C.白色念珠菌。添加抗前列腺素或抗血栓烷抗体血清单独抑制芽管形成近30%，而对照抗体没有影响，表明这些类花生酸是血清中的主要形态发生因子。由于这些分子也与白蛋白结合，这也可以解释与白蛋白相关的血清中的菌丝转化活性。有趣的是，短链脂肪酸（丁酸），乳酸菌（LAB）的产品，抑制发芽。此外，乳酸菌培养上清以及活乳酸菌也能抑制C。白色念珠菌形态发生总的来说，这些结果表明，脂肪酸代谢产物和脂肪酸途径可以上调和下调白念珠菌的萌发。
Candida albicans is an opportunistic dimorphic fungus that inhabits various host mucosal sites. Conversion from the yeast to the hyphal form has been associated with increased virulence and mucosal invasiveness. C. albicans morphogenesis is regulated by multiple signals and signaling pathways. However, signals that control morphogenesis in vivo are unknown. We investigated the effects of host long chain fatty acids, eicosanoids, and bacterial short chain fatty acids on control of germination. None of the C-18 or C-20 fatty acids tested had an effect on enhancing germ tube formation (arachidonic acid, oleic acid, linolenic acid, or gamma-linolenic acid). Among the different eicosanoids, both prostaglandin E-2 and thromboxane B-2 significantly enhanced serum-induced germination by C. albicans. Addition of antiprostaglandin or antithromboxane antibodies to serum alone inhibited germ tube formation by almost 30%, while control antibody had no effect, indicating that these eicosanoids are major morphogenic factors in the serum. Since these molecules also bind to albumin, this may also explain the hyphal transforming activity in serum that associates with albumin. Interestingly, short chain fatty acids (butyric acid), the product of lactic acid bacteria (LAB), inhibited germination. In addition, LAB culture supernatants as well as live LAB also inhibited C. albicans morphogenesis. Overall, these results indicate that fatty acid metabolites and fatty acid pathways can up-regulate and down-regulate germination in C albicans.