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乙醛酸循环基因 ICL1 是光滑念珠菌代谢灵活性和毒力所必需的。

Glyoxylate cycle gene ICL1 is essential for the metabolic flexibility and virulence of Candida glabrata.

机构信息

Department of Medical Microbiology and Parasitology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia.

Department of Pathology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 UPM, Serdang, Selangor, Malaysia.

出版信息

Sci Rep. 2019 Feb 26;9(1):2843. doi: 10.1038/s41598-019-39117-1.

DOI:10.1038/s41598-019-39117-1
PMID:30808979
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6391369/
Abstract

The human fungal pathogen Candida glabrata appears to utilise unique stealth, evasion and persistence strategies in subverting the onslaught of host immune response during systemic infection. However, macrophages actively deprive the intracellular fungal pathogen of glucose, and therefore alternative carbon sources probably support the growth and survival of engulfed C. glabrata. The present study aimed to investigate the role of the glyoxylate cycle gene ICL1 in alternative carbon utilisation and its importance for the virulence of C. glabrata. The data showed that disruption of ICL1 rendered C. glabrata unable to utilise acetate, ethanol or oleic acid. In addition, C. glabrata icl1∆ cells displayed significantly reduced biofilm growth in the presence of several alternative carbon sources. It was also found that ICL1 is crucial for the survival of C. glabrata in response to macrophage engulfment. Disruption of ICL1 also conferred a severe attenuation in the virulence of C. glabrata in the mouse model of invasive candidiasis. In conclusion, a functional glyoxylate cycle is essential for C. glabrata to utilise certain alternative carbon sources in vitro and to display full virulence in vivo. This reinforces the view that antifungal drugs that target fungal Icl1 have potential for future therapeutic intervention.

摘要

人类真菌病原体光滑念珠菌似乎利用独特的隐身、逃避和持久策略，在系统性感染中颠覆宿主免疫反应的攻击。然而，巨噬细胞积极剥夺细胞内真菌病原体的葡萄糖，因此替代碳源可能支持吞噬的光滑念珠菌的生长和存活。本研究旨在探讨乙醛酸循环基因 ICL1 在替代碳利用中的作用及其对光滑念珠菌毒力的重要性。研究数据表明，ICL1 的缺失使光滑念珠菌无法利用乙酸盐、乙醇或油酸。此外，在存在几种替代碳源的情况下，ICL1 缺失的光滑念珠菌细胞的生物膜生长明显减少。还发现 ICL1 对巨噬细胞吞噬作用下光滑念珠菌的存活至关重要。ICL1 的缺失也导致光滑念珠菌在侵袭性念珠菌病小鼠模型中的毒力严重减弱。总之，功能性乙醛酸循环对于光滑念珠菌在体外利用某些替代碳源并在体内表现出完全毒力是必不可少的。这进一步证实了靶向真菌 Icl1 的抗真菌药物具有未来治疗干预的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b3/6391369/3be07c0015c7/41598_2019_39117_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b3/6391369/b8500a8a3880/41598_2019_39117_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b3/6391369/98e46838e3d5/41598_2019_39117_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b3/6391369/35e21197c749/41598_2019_39117_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b3/6391369/f5fb5ab9933e/41598_2019_39117_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b3/6391369/9db9bfb27163/41598_2019_39117_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b3/6391369/3be07c0015c7/41598_2019_39117_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b3/6391369/b8500a8a3880/41598_2019_39117_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b3/6391369/98e46838e3d5/41598_2019_39117_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b3/6391369/35e21197c749/41598_2019_39117_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b3/6391369/f5fb5ab9933e/41598_2019_39117_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b3/6391369/9db9bfb27163/41598_2019_39117_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59b3/6391369/3be07c0015c7/41598_2019_39117_Fig6_HTML.jpg

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