[1] TASAKI S, CHO T, NAGAO J I, et al. Th17 cells differentiated with mycelial membranes of Candida albicans prevent oral candidiasis[J]. FEMS Yeast Res,2018,18(3):foy018.
[2] LOPES J P, LIONAKIS M S. Pathogenesis and virulence of Candida albicans[J]. Virulence, 2022,13(1):89-121.
[3] 钟慧婷,佘晓东,刘维达.宿主对白念珠菌的免疫机制进展[J].中国真菌学杂志,2017,12(6):375-377.
[4] BACHER P, HOHNSTEIN T, BEERBAUM E, et al. Human anti-fungal Th17 immunity and pathology rely on cross-reactivity against Candida albicans[J]. Cell,2019,176(6):1340-1355.e15.
[5] VONK A G, NETEA M G, VAN DER MEER J W, et al. Host defence against disseminated Candida albicans infection and implications for antifungal immunotherapy[J]. Expert Opin Biol Ther,2006,6(9):891-903.
[6] AUSTERMEIER S, KASPER L, WESTMAN J, et al. I want to break free-macrophage strategies to recognize and kill Candida albicans, and fungal counter-strategies to escape[J]. Curr Opin Microbiol,2020,58:15-23. DOI: 10.1016/j.mib.2020.05.007.
[7] NGO L Y, KASAHARA S, KUMASAKA D K, et al. Inflammatory monocytes mediate early and organ-specific innate defense during systemic candidiasis[J]. J Infect Dis, 2014,209(1):109-119.
[8] ERWIG L P, GOW N A. Interactions of fungal pathogens with phagocytes[J]. Nat Rev Microbiol,2016,14(3):163-176.
[9] WESTMAN J, WALPOLE G F W, et al. Lysosome fusion maintains phagosome integrity during fungal infection[J]. Cell Host Microbe,2020,28(6):798-812.
[10] PRICE J V, VANCE R E. The macrophage paradox[J]. Immunity, 2014,41(5):685-693.
[11] WALPOLE G F W, PLUMB J D, CHUNG D, et al.Inactivation of Rho GTPases by burkholderia cenocepacia induces a wash-mediated actin polymerization that delays phagosome maturation[J] Cell Rep,2020,31(9):107721.
[12] FLANNAGAN R S, HEIT B, HEINRICHS D E. Intracellular replication of Staphylococcus aureus in mature phagolysosomes in macrophages precedes host cell death, and bacterial escape and dissemination[J]. Cell Microbiol,2016,18(4):514-535.
[13] WESTMAN J, MORAN G, MOGAVERO S, et al. Candida albicans hyphal expansion causes phagosomal membrane damage and luminal alkalinization[J]. mBio, 2018,9(5):e01226-18.
[14] OLIVIER FAB, HILSENSTEIN V, WEERASINGHE H, etal.The escape of Candida albicans from macrophages is enabled by the fungal toxin candidalysin and two host cell death pathways[J]. Cell Rep, 2022,40(12):111374.
[15] BANOTH B, TULADHAR S, KARKI R, et al.ZBP1 promotes fungi-inducedinflammasome activation and pyroptosis, apoptosis, and necroptosis (PANoptosis)[J]. J Biol Chem, 2020, 295(52): 18276-18283.
[16] LOUREIRO A, PAIS C, SAMPAIO P. Relevance of macrophage extracellular traps in C. albicans killing[J]. Front Immunol,2019,10:2767.DOI: 10.3389/fimmu.2019.02767.
[17] RASMUSSEN K H, HAWKINS C L. Role of macrophage extracellular traps ininnate immunity and inflammatory disease[J]. Biochem Soc Trans,2022,50(1):21-32.
[18] PAPAYANNOPOULOS V.Neutrophil extracellular traps in immunity and disease[J]. Nat Rev Immunol,2018,18(2):134-147.
[19] URBAN C F, REICHARD U, BRINKMANN V, et al.Neutrophil extracellular traps capture and kill Candida albicans yeast and hyphal forms[J]. Cell Microbiol, 2006, 8(4): 668-676.
[20] KING P T, SHARMA R, O'SULLIVAN K M, et al. Deoxyribonuclease 1 reduces pathogenic effects of cigarette smoke exposure in the lung[J]. Sci Rep,2017,7(1):12128.
[21] RAYNER B S, ZHANG Y, BROWN B E, et al. Role ofhypochlorous acid (HOCl) and other inflammatory mediators in the induction of macrophage extracellular trap formation[J]. Free Radic Biol Med, 2018,129:25-34. DOI: 10.1016/j.freeradbiomed.2018.09.001.
[22] URBAN C F, ERMERT D, SCHMID M, et al. Neutrophil extracellular traps contain calprotectin, a cytosolic protein complex involved in host defense against Candida albicans[J]. PLoS Pathog,2009,5(10):e1000639.
[23] MCCORMICK A, HEESEMANN L, WAGENER J, et al. NETs formed by humanneutrophils inhibit growth of the pathogenic mold Aspergillus fumigatus[J]. Microbes Infect, 2010,12(12-13):928-936.[24] DE PAULA MENEZES R, DE MELO RICETO É B, BORGES A S, et al. Evaluation of virulence factors of Candida albicans isolated from HIV-positive individuals using HAART[J]. Arch Oral Biol,2016,66:61-65.DOI: 10.1016/j.archoralbio.2016.02.004. [25] ZHANG X, ZHAO S, SUN L, et al. Different virulence of Candida albicans is attributed to the ability of escape from neutrophil extracellular traps by secretion of DNase[J]. Am J Transl Res, 2017,9(1):50-62. [26] JE S, QUAN H, YOON Y, et al. Mycobacterium massiliense induces macrophage extracellular traps with facilitating bacterial growth[J]. PLoS One,2016,11(5):e0155685. [27] KIM Y G, LEE J H, PARK S, et al.Hydroquinones including tetrachlorohydroquinone inhibit Candida albicans biofilm formation by repressing hyphae-related genes[J]. Microbiol Spectr,2022,10(5):e0253622. [28] SUDBERY P E. Growth of Candida albicans hyphae[J]. Nat Rev Microbiol, 2011,9(10):737-748. [29] RICHARDSON J P, HO J, NAGLIK J R. Candida-epithelial interactions[J]. J Fungi (Basel),2018,4(1):22. [30] MOYES D L, RICHARDSON J P, NAGLIK J R. Candida albicans-epithelial interactions and pathogenicity mechanisms: scratching the surface[J]. Virulence,2015,6(4):338-346. [31] ALLERT S, FÖRSTER T M, SVENSSON C M, et al. Candida albicans-induced epithelial damage mediates translocation through intestinal barriers[J]. mBio,2018,9(3):e00915-18. [32] WILSON D, NAGLIK J R, HUBE B. The missing link between Candida albicans hyphal morphogenesis and host cell damage[J]. PLoS Pathog,2016,12(10):e1005867. [33] MOYES D L, WILSON D, RICHARDSON J P, et al. Candidalysin is a fungal peptide toxin critical for mucosal infection[J]. Nature,2016,532(7597):64-68. [34] ROGIERS O, FRISING U C, KUCHARÍKOVÁ S, et al. Candidalysin crucially contributes to Nlrp3 inflammasome activation by Candida albicans Hyphae[J]. mBio,2019,10(1):e02221-18. [35] KASPER L, KÖNIG A, KOENIG P A, et al. The fungal peptide toxincandidalysin activates the NLRP3 inflammasome and causes cytolysis in mononuclear phagocytes[J]. Nat Commun,2018,9(1):4260. |
