白念珠菌细胞壁结构及其与宿主相互作用的研究进展

doi:10.3969/j.issn.1674-8115.2021.09.017

上海交通大学学报(医学版) ›› 2021, Vol. 41 ›› Issue (9): 1246-1251.doi: 10.3969/j.issn.1674-8115.2021.09.017

• 综述 • 上一篇

白念珠菌细胞壁结构及其与宿主相互作用的研究进展

梅一堃(), 谭镜璁, 王安君, 王慧, 刘宁宁()

上海交通大学公共卫生学院，上海 200025

收稿日期:2020-06-30 出版日期:2021-08-24 发布日期:2021-08-24
通讯作者: 刘宁宁 E-mail:1558685903@qq.com;liuningning@shsmu.edu.cn
作者简介:梅一堃（1992—），男，硕士生；电子信箱：1558685903@qq.com。
基金资助:
国家重点研发计划(2018YFC2000700);国家自然科学基金(31900129);上海高校青年东方学者计划(QD2018016);上海浦江人才计划(18PJ1406600);上海交通大学医学与工程交叉学科研究基金(YG2020YQ06)

Advances in cell wall structure and Candida albicans-host interaction

Yi-kun MEI(), Jing-cong TAN, An-jun WANG, Hui WANG, Ning-ning LIU()

School of Public Health, Shanghai Jiao Tong University, Shanghai 200025, China

Received:2020-06-30 Online:2021-08-24 Published:2021-08-24
Contact: Ning-ning LIU E-mail:1558685903@qq.com;liuningning@shsmu.edu.cn
Supported by:
National Key R&D Program of China(2018YFC2000700);National Natural Science Foundation of China(31900129);Program for Young Eastern Scholar at Shanghai Institutions of Higher Learning(QD2018016);Shanghai Pujiang Program(18PJ1406600);Medicine and Engineering Interdisciplinary Research Fund of Shanghai Jiao Tong University(YG2020YQ06)

摘要/Abstract

摘要：

白念珠菌是常见的人体条件致病真菌，其侵染人体造成的血液感染死亡率高达40%，在癌症患者中致死率高达70%，极大地增加了人体健康负担。白念珠菌细胞壁是抵御外界侵害的第一道防线，是真菌与宿主接触的第一靶点，因此细胞壁结构对于真菌-宿主相互作用以及宿主免疫识别至关重要，是抗真菌治疗极具前景的靶点之一。当白念珠菌细胞壁的完整性遭受破坏时，细胞壁的分子结构就会受到干扰，从而导致细胞裂解和死亡。该文综述了白念珠菌细胞壁各成分的特点及其对真菌-宿主相互作用和免疫识别作用机制的影响，以期为寻找治疗白念珠菌感染的特异性靶点、筛选或鉴定更多经济有效的抗真菌药物提供新的研究线索和理论依据。

关键词: 白念珠菌, 细胞壁, 真菌-宿主相互作用, 免疫识别, 抗真菌药物

Abstract:

Candida albicans is an opportunistic human fungal pathogen. The mortality rate of blood infection caused by Candida albicans is as high as 40% while that of the cancer patients can even reach to 70%, which greatly increases the burden of human health. The cell wall of Candida albicans is the frontline of defense against external stress and the first contact point between fungi and host. Therefore, the cell wall is very important for fungi-host interaction and immune recognition, and is the most attractive target for antifungal therapy. Once the balance of synthesis and remodeling of cell wall of Candida albicans is broken, the molecular integrity of cell wall will be disturbed, which will finally lead to cell lysis and death. This paper reviews the characteristics of cell wall components of Candida albicans and their functions on fungi-host interaction and immune recognition mechanism, in order to provide novel research clues and theoretical basis for identification of specific antifungal targets and development of more economic and effective antifungal drugs.

Key words: Candida albicans, cell wall, fungi-host interaction, immune recognition, antifungal agent

中图分类号:

R379.4

梅一堃, 谭镜璁, 王安君, 王慧, 刘宁宁. 白念珠菌细胞壁结构及其与宿主相互作用的研究进展[J]. 上海交通大学学报(医学版), 2021, 41(9): 1246-1251.

Yi-kun MEI, Jing-cong TAN, An-jun WANG, Hui WANG, Ning-ning LIU. Advances in cell wall structure and Candida albicans-host interaction[J]. JOURNAL OF SHANGHAI JIAOTONG UNIVERSITY (MEDICAL SCIENCE), 2021, 41(9): 1246-1251.

参考文献 50

1	Tasaki S, Cho T, Nagao JI, et al. Th17 cells differentiated with mycelial membranes of Candida albicans prevent oral candidiasis[J]. FEMS Yeast Res, 2018, 18(3).
2	Bongomin F, Gago S, Oladele RO, et al. Global and multi-national prevalence of fungal diseases-estimate precision[J]. J Fungi (Basel), 2017, 3(4): E57.
3	Jabra-Rizk MA, Kong EF, Tsui C, et al. Candida albicans pathogenesis: fitting within the host-microbe damage response framework[J]. Infect Immun, 2016, 84(10): 2724-2739.
4	Gabrielli E, Sabbatini S, Roselletti E, et al. In vivo induction of neutrophil chemotaxis by secretory aspartyl proteinases of Candida albicans[J]. Virulence, 2016, 7(7): 819-825.
5	Yano J, Palmer GE, Eberle KE, et al. Vaginal epithelial cell-derived S100 alarmins induced by Candida albicansvia pattern recognition receptor interactions are sufficient but not necessary for the acute neutrophil response during experimental vaginal candidiasis[J]. Infect Immun, 2014, 82(2): 783-792.
6	Poulain D. Candida albicans, plasticity and pathogenesis[J]. Crit Rev Microbiol, 2015, 41(2): 208-217.
7	Pradhan A, Avelar GM, Bain JM, et al. Hypoxia promotes immune evasion by triggering β-glucan masking on the Candida albicans cell surface via mitochondrial and cAMP-protein kinase A signaling[J]. mBio, 2018, 9(6): e01318-18.
8	Shepherd MG. Cell envelope of Candida albicans[J]. Crit Rev Microbiol, 1987, 15(1): 7-25.
9	Rigamonti M, Groppi S, Belotti F, et al. Hypotonic stress-induced calcium signaling in Saccharomyces cerevisiae involves TRP-like transporters on the endoplasmic reticulum membrane[J]. Cell Calcium, 2015, 57(2): 57-68.
10	Ishida Y, Ohta K, Naruse T, et al. Candida albicans β-glucan-containing particles increase HO-1 expression in oral keratinocytes via a reactive oxygen species/p38 mitogen-activated protein kinase/Nrf2 pathway[J]. Infect Immun, 2018, 86(4): e00575-17.
11	Canabarro A, Valle C, Farias MR, et al. Association of subgingival colonization of Candida albicans and other yeasts with severity of chronic periodontitis[J]. J Periodontal Res, 2013, 48(4): 428-432.
12	Lopes JP, Stylianou M, Backman E, et al. Evasion of immune surveillance in low oxygen environments enhances Candida albicans virulence[J]. mBio, 2018, 9(6): e02120-18.
13	Lowman DW, Greene RR, Bearden DW, et al. Novel structural features in Candida albicans hyphal glucan provide a basis for differential innate immune recognition of hyphae versus yeast[J]. J Biol Chem, 2014, 289(6):3432-3443.
14	Ferwerda B, Ferwerda G, Plantinga TS, et al. Human dectin-1 deficiency and mucocutaneous fungal infections[J]. N Engl J Med, 2009,361(18):1760-1767.
15	Gantner BN, Simmons RM, Underhill DM. Dectin-1 mediates macrophage recognition of Candida albicans yeast but not filaments[J]. EMBO J, 2005,24(6):1277-1286.
16	Wheeler RT, Kombe D, Agarwala SD, et al. Dynamic, morphotype-specific Candida albicans β-glucan exposure during infection and drug treatment[J]. PLoS Pathog, 2008, 4(12): e1000227.
17	Gow NA, Netea MG, Munro CA, et al. Immune recognition of Candida albicans β-glucan by dectin-1[J]. J Infect Dis, 2007, 196(10): 1565-1571.
18	Klippel N, Cui SN, Groebe L, et al. Deletion of the Candida albicans histidine kinase gene CHK1 improves recognition by phagocytes through an increased exposure of cell wall β-1,3-glucans[J]. Microbiology, 2010, 156(11): 3432-3444.
19	Marakalala MJ, Vautier S, Potrykus J, et al. Differential adaptation of Candida albicansin vivo modulates immune recognition by dectin-1[J]. PLoS Pathog, 2013, 9(4): e1003315.
20	Denning DW. Echinocandin antifungal drugs[J]. Lancet, 2003, 362(9390): 1142-1151.
21	Liu NN, Acosta-Zaldívar M, Qi WJ, et al. Phosphoric metabolites link phosphate import and polysaccharide biosynthesis for Candida albicans cell wall maintenance[J]. mBio, 2020, 11(2): e03225-19.
22	Cambi A, Netea MG, Mora-Montes HM, et al. Dendritic cell interaction with Candida albicans critically depends on N-linked mannan[J]. J Biol Chem, 2008, 283(29): 20590-20599.
23	de Groot PW, de Boer AD, Cunningham J, et al. Proteomic analysis of Candida albicans cell walls reveals covalently bound carbohydrate-active enzymes and adhesins[J]. Eukaryot Cell, 2004, 3(4): 955-965.
24	Richard M, de Groot P, Courtin O, et al. GPI7 affects cell-wall protein anchorage in Saccharomyces cerevisiae and Candida albicans[J]. Microbiology, 2002, 148(7): 2125-2133.
25	Klis FM, Sosinska GJ, de Groot PW, et al. Covalently linked cell wall proteins of Candida albicans and their role in fitness and virulence[J]. FEMS Yeast Res, 2009, 9(7): 1013-1028.
26	Bartkeviciūte D, Sasnauskas K. Disruption of the MNN10 gene enhances protein secretion in Kluyveromyces lactis and Saccharomyces cerevisiae[J]. FEMS Yeast Res, 2004, 4(8): 833-840.
27	Zhang SQ, Zou Z, Shen H, et al. Mnn10 maintains pathogenicity in Candida albicans by extending α-1, 6-mannose backbone to evade host dectin-1 mediated antifungal immunity[J]. PLoS Pathog, 2016, 12(5): e1005617.
28	Lin J, Wester MJ, Graus MS, et al. Nanoscopic cell-wall architecture of an immunogenic ligand in Candida albicans during antifungal drug treatment[J]. Mol Biol Cell, 2016, 27(6): 1002-1014.
29	Graus MS, Wester MJ, Lowman DW, et al. Mannan molecular substructures control nanoscale glucan exposure in Candida[J]. Cell Rep, 2018, 24(9): 2432-2442.e5.
30	Bain JM, Louw J, Lewis LE, et al. Candida albicans hypha formation and mannan masking of β-glucan inhibit macrophage phagosome maturation[J]. mBio, 2014, 5(6): e01874.
31	Dutton LC, Nobbs AH, Jepson K, et al. O-mannosylation in Candida albicans enables development of interkingdom biofilm communities[J]. mBio, 2014, 5(2): e00911.
32	Munro CA, Gow NA. Chitin synthesis in human pathogenic fungi[J]. Med Mycol, 2001, 39(): 41-53.
33	Kapteyn JC, Hoyer LL, Hecht JE, et al. The cell wall architecture of Candida albicans wild-type cells and cell wall-defective mutants[J]. Mol Microbiol, 2000, 35(3): 601-611.
34	Hasim S, Allison DP, Retterer ST, et al. β-(1, 3)-glucan unmasking in some Candida albicans mutants correlates with increases in cell wall surface roughness and decreases in cell wall elasticity[J]. Infect Immun, 2017, 85(1): e00601-16.
35	Cabib E. Two novel techniques for determination of polysaccharide cross-links show that Crh1p and Crh2p attach chitin to both β(1-6)- and β(1-3)glucan in the Saccharomyces cerevisiae cell wall[J]. Eukaryot Cell, 2009, 8(11): 1626-1636.
36	Ene IV, Heilmann CJ, Sorgo AG, et al. Carbon source-induced reprogramming of the cell wall proteome and secretome modulates the adherence and drug resistance of the fungal pathogen Candida albicans[J]. Proteomics, 2012, 12(21): 3164-3179.
37	Cantarel BL, Coutinho PM, Rancurel C, et al. The Carbohydrate-Active EnZymes database (CAZy): an expert resource for glycogenomics[J]. Nucleic Acids Res, 2009, 37(database issue): D233-D238.
38	Munro CA, Selvaggini S, de Bruijn I, et al. The PKC, HOG and Ca²⁺ signalling pathways co-ordinately regulate chitin synthesis in Candida albicans[J]. Mol Microbiol, 2007, 63(5): 1399-1413.
39	Cottier F, Sherrington S, Cockerill S, et al. Remasking of Candida albicans β-glucan in response to environmental pH is regulated by quorum sensing[J]. mBio, 2019, 10(5): e02347-19.
40	Swidsinski A, Guschin A, Tang Q, et al. Vulvovaginal candidiasis: histologic lesions are primarily polymicrobial and invasive and do not contain biofilms[J]. Am J Obstet Gynecol, 2019, 220(1): 91.e1-91.e8.
41	Heilmann CJ, Sorgo AG, Mohammadi S, et al. Surface stress induces a conserved cell wall stress response in the pathogenic fungus Candida albicans[J]. Eukaryot Cell, 2013, 12(2): 254-264.
42	Hardison SE, Brown GD. C-type lectin receptors orchestrate antifungal immunity[J]. Nat Immunol, 2012,13(9): 817-822.
43	Wagener J, MacCallum DM, Brown GD, et al. Candida albicans chitin increases arginase-1 activity in human macrophages, with an impact on macrophage antimicrobial functions[J]. mBio, 2017, 8(1): e01820-16.
44	Latgé JP. Tasting the fungal cell wall[J]. Cell Microbiol, 2010, 12(7): 863-872.
45	Rocha MC, Fabri JH, Franco de Godoy K, et al. Aspergillus fumigatus MADS-box transcription factor rlmA is required for regulation of the cell wall integrity and virulence[J]. G3 (Bethesda), 2016, 6(9): 2983-3002.
46	Román E, Arana DM, Nombela C, et al. MAP kinase pathways as regulators of fungal virulence[J]. Trends Microbiol, 2007, 15(4): 181-190.
47	Navarro-García F, Eisman B, Fiuza SM, et al. The MAP kinase Mkc1p is activated under different stress conditions in Candida albicans[J]. Microbiology (Reading), 2005, 151(Pt 8): 2737-2749.
48	Liu NN, Uppuluri P, Broggi A, et al. Intersection of phosphate transport, oxidative stress and TOR signalling in Candida albicans virulence[J]. PLoS Pathog, 2018, 14(7): e1007076.
49	Enjalbert B, Smith DA, Cornell MJ, et al. Role of the Hog1 stress-activated protein kinase in the global transcriptional response to stress in the fungal pathogen Candida albicans[J]. Mol Biol Cell, 2006, 17(2): 1018-1032.
50	Galán-Díez M, Arana DM, Serrano-Gómez D, et al. Candida albicans β-glucan exposure is controlled by the fungal CEK1-mediated mitogen-activated protein kinase pathway that modulates immune responses triggered through dectin-1[J]. Infect Immun, 2010,78(4): 1426-1436.

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白念珠菌细胞壁结构及其与宿主相互作用的研究进展

Advances in cell wall structure and Candida albicans-host interaction

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