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Immune Sensing of Candida albicans

Bojang, Ebrima, Ghuman, Harlene, Kumwenda, Pizga, Hall, Rebecca A.·2021·Journal of Fungi
DOI 10.3390/jof7020119
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Abstract

Candida albicans infections range from superficial to systemic and are one of the leading causes of fungus-associated nosocomial infections. The innate immune responses during these various infection types differ, suggesting that the host environment plays a key role in modulating the host–pathogen interaction. In addition, C. albicans is able to remodel its cell wall in response to environmental conditions to evade host clearance mechanisms and establish infection in niches, such as the oral and vaginal mucosa. Phagocytes play a key role in clearing C. albicans, which is primarily mediated by Pathogen Associated Molecular Pattern (PAMP)–Pattern Recognition Receptor (PRR) interactions. PRRs such as Dectin-1, DC-SIGN, and TLR2 and TLR4 interact with PAMPs such as β-glucans, N-mannan and O-mannan, respectively, to trigger the activation of innate immune cells. Innate immune cells exhibit distinct yet overlapping repertoires of PAMPs, resulting in the preferential recognition of particular Candida morphotypes by them. The role of phagocytes in the context of individual infection types also differs, with neutrophils playing a prominent role in kidney infections, and dendritic cells playing a prominent role in skin infections. In this review, we provide an overview of the key receptors involved in the detection of C. albicans and discuss the differential innate immune responses to C. albicans seen in different infection types such as vulvovaginal candidiasis (VVC) and oral candidiasis.

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Research works printed but not linked: 131

  1. Ward, 2017, Infant fungal communities: Current knowledge and research opportunities, BMC Med., 15, 30, 10.1186/s12916-017-0802-z · DOI
  2. Tso, G.H.W., Reales-Calderon, J.A., and Pavelka, N. (2018). The elusive anti-Candida vaccine: Lessons from the past and opportunities for the future. Front. Immunol., 9. · DOI
  3. Moyes, 2016, Candidalysin is a fungal peptide toxin critical for mucosal infection, Nature, 532, 64, 10.1038/nature17625 · DOI
  4. Zhu, 2010, Interactions of Candida albicans with epithelial cells, Cell. Microbiol., 12, 273, 10.1111/j.1462-5822.2009.01412.x · DOI · Paper page
  5. Gregorio, 2019, Biofilms and vulvovaginal candidiasis, Coll. Surf. B Biointerfaces, 174, 110, 10.1016/j.colsurfb.2018.11.011 · DOI
  6. Du, Q., Ren, B., He, J., Peng, X., Guo, Q., Zheng, L., Li, J., Dai, H., Chen, V., and Zhang, L. (2020). Candida albicans promotes tooth decay by inducing oral microbial dysbiosis. ISME J. · DOI
  7. Hall, 2015, Dressed to impress: Impact of environmental adaptation on the Candida albicans cell wall, Mol. Microbiol., 97, 7, 10.1111/mmi.13020 · DOI
  8. Gow, N.A.R., Latge, J.-P., and Munro, C.A. (2017). The Fungal cell wall: Structure, biosynthesis, and function. Microbiol. Spectr., 5. · DOI · Paper page
  9. Chen, 2017, Dectin-1 plays an important role in host defense against systemic Candida glabrata infection, Virulence, 8, 1643, 10.1080/21505594.2017.1346756 · DOI
  10. Esteban, 2011, Fungal recognition is mediated by the association of dectin-1 and galectin-3 in macrophages, Proc. Nat. Acad. Sci. USA, 108, 14270, 10.1073/pnas.1111415108 · DOI
  11. Gantner, 2005, Dectin-1 mediates macrophage recognition of Candida albicans yeast but not filaments, EMBO J., 24, 1277, 10.1038/sj.emboj.7600594 · DOI
  12. Li, 2011, The β-glucan receptor Dectin-1 activates the integrin Mac-1 in neutrophils via Vav protein signaling to promote Candida albicans clearance, Cell Host Microbe, 10, 603, 10.1016/j.chom.2011.10.009 · DOI
  13. Ifrim, 2016, The role of dectin-2 for host defense against disseminated Candidiasis, J. Interferon Cytokine Res. Off. J. Int. Soc. Interferon Cytokine Res., 36, 267, 10.1089/jir.2015.0040 · DOI
  14. Saijo, 2010, Dectin-2 recognition of alpha-mannans and induction of Th17 cell differentiation is essential for host defense against Candida albicans., Immunity, 32, 681, 10.1016/j.immuni.2010.05.001 · DOI
  15. Zhu, 2013, C-type lectin receptors Dectin-3 and Dectin-2 form a heterodimeric pattern-recognition receptor for host defense against fungal infection, Immunity, 39, 324, 10.1016/j.immuni.2013.05.017 · DOI
  16. Cambi, 2003, The C-type lectin DC-SIGN (CD209) is an antigen-uptake receptor for Candida albicans on dendritic cells, Eur. J. Immunol., 33, 532, 10.1002/immu.200310029 · DOI
  17. Cambi, 2008, Dendritic cell interaction with Candida albicans critically depends on N-linked mannan, J. Biol. Chem., 283, 20590, 10.1074/jbc.M709334200 · DOI
  18. Wells, 2008, The macrophage-inducible C-type lectin, mincle, is an essential component of the innate immune response to Candida albicans., J. immunol., 180, 7404, 10.4049/jimmunol.180.11.7404 · DOI
  19. Netea, 2006, Immune sensing of Candida albicans requires cooperative recognition of mannans and glucans by lectin and Toll-like receptors, J. Clin. Investig., 116, 1642, 10.1172/JCI27114 · DOI
  20. Marijnissen, 2009, The macrophage mannose receptor induces IL-17 in response to Candida albicans., Cell Host Microbe, 5, 329, 10.1016/j.chom.2009.02.006 · DOI
  21. Blasi, 2005, Biological importance of the two Toll-like receptors, TLR2 and TLR4, in macrophage response to infection with Candida albicans., FEMS Immunol. Med. Microbiol., 44, 69, 10.1016/j.femsim.2004.12.005 · DOI
  22. Tessarolli, 2010, Absence of TLR2 influences survival of neutrophils after infection with Candida albicans., Med. Mycol., 48, 129, 10.3109/13693780902964339 · DOI
  23. Jouault, 2003, Candida albicans phospholipomannan is sensed through toll-like receptors, J. Infect. Dis., 188, 165, 10.1086/375784 · DOI · Paper page
  24. Netea, 2008, Role of TLR1 and TLR6 in the host defense against disseminated candidiasis, FEMS Immunol. Med. Microbiol., 52, 118, 10.1111/j.1574-695X.2007.00353.x · DOI
  25. Halder, 2020, Immune modulation by complement receptor 3-dependent human monocyte TGF-β1-transporting vesicles, Nat. Commun., 11, 2331, 10.1038/s41467-020-16241-5 · DOI
  26. Levin, 2016, The life cycle of phagosomes: Formation, maturation, and resolution, Immunol. Rev., 273, 156, 10.1111/imr.12439 · DOI
  27. Mukaremera, 2017, Candida albicans yeast, pseudohyphal, and hyphal morphogenesis differentially affects immune recognition, Front. Immunol., 8, 629, 10.3389/fimmu.2017.00629 · DOI
  28. Hopke, A., Nicke, N., Hidu, E.E., Degani, G., Popolo, L., and Wheeler, R.T. (2016). Neutrophil Attack triggers extracellular trap-dependent Candida cell wall remodeling and altered immune recognition. PLoS Pathog., 12. · DOI · Paper page
  29. Bacci, 2000, Dendritic cells discriminate between yeasts and hyphae of the fungus Candida albicans. Implications for initiation of T helper cell immunity in vitro and in vivo, J. Exp. Med., 191, 1661, 10.1084/jem.191.10.1661 · DOI
  30. Hope, 2007, Effect of neutropenia and treatment delay on the response to antifungal agents in experimental disseminated candidiasis, Antimicrob. Agents Chemother., 51, 285, 10.1128/AAC.00601-06 · DOI
  31. Ramy, 2017, Role of early onset neutropenia in development of Candidemia in premature infants, J. Trop. Pediatr., 64, 51, 10.1093/tropej/fmx029 · DOI
  32. Son, H.-J., Kim, M.J., Lee, S., Choi, S., Jung, K.H., Jung, J., Chong, Y.P., Kim, S.-H., Choi, S.-H., and Kim, Y.S. (2019). Risk factors and outcomes of patients with ocular involvement of candidemia. PLoS ONE, 14. · DOI
  33. Fradin, 2005, Granulocytes govern the transcriptional response, morphology and proliferation of Candida albicans in human blood, Mol. Microbiol., 56, 397, 10.1111/j.1365-2958.2005.04557.x · DOI · Paper page
  34. Newman, 2001, Candida albicans is phagocytosed, killed, and processed for antigen presentation by human dendritic cells, Infect. Immun., 69, 6813, 10.1128/IAI.69.11.6813-6822.2001 · DOI
  35. Brown, 2001, A new receptor for β-glucans, Nature, 413, 36, 10.1038/35092620 · DOI · Paper page
  36. Erwig, 2016, Interactions of fungal pathogens with phagocytes, Nat. Rev. Microbiol., 14, 163, 10.1038/nrmicro.2015.21 · DOI · Paper page
  37. Thornton, 1996, Analysis of the sugar specificity and molecular location of the beta-glucan-binding lectin site of complement receptor type 3 (CD11b/CD18), J. Immunol., 156, 1235, 10.4049/jimmunol.156.3.1235 · DOI
  38. Mazzolini, 2016, Dynamin-actin cross talk contributes to phagosome formation and closure, Traffic, 17, 487, 10.1111/tra.12386 · DOI
  39. Gold, 1999, Dynamin 2 is required for phagocytosis in macrophages, J. Exp. Med., 190, 1849, 10.1084/jem.190.12.1849 · DOI
  40. Campellone, 2010, A nucleator arms race: Cellular control of actin assembly, Nat. Rev. Mol. Cell Biol., 11, 237, 10.1038/nrm2867 · DOI
  41. Lee, 2003, Phagocytosis by neutrophils, Microb. Infect., 5, 1299, 10.1016/j.micinf.2003.09.014 · DOI
  42. Grinstein, 2002, Signaling to localized degranulation in neutrophils adherent to immune complexes, J. Leukoc. Biol., 71, 701, 10.1189/jlb.71.4.701 · DOI
  43. Nordenfelt, 2011, Phagosome dynamics during phagocytosis by neutrophils, J. Leukoc. Biol., 90, 271, 10.1189/jlb.0810457 · DOI
  44. Roberts, 2000, Dynamics of Rab5 activation in endocytosis and phagocytosis, J. Leukoc. Biol., 68, 627, 10.1189/jlb.68.5.627 · DOI
  45. Vieira, 2003, Modulation of Rab5 and Rab7 recruitment to phagosomes by phosphatidylinositol 3-kinase, Mol. Cell. Biol., 23, 2501, 10.1128/MCB.23.7.2501-2514.2003 · DOI
  46. Vylkova, S., and Lorenz, M.C. (2014). Modulation of phagosomal pH by Candida albicans promotes hyphal morphogenesis and requires Stp2p, a regulator of amino acid transport. PLoS Pathog., 10. · DOI · Paper page
  47. Canton, 2014, Contrasting phagosome pH regulation and maturation in human M1 and M2 macrophages, Mol. Biol. Cell, 25, 3330, 10.1091/mbc.e14-05-0967 · DOI · Paper page
  48. Jankowski, 2002, Determinants of the phagosomal pH in neutrophils, J. Biol. Chem., 277, 6059, 10.1074/jbc.M110059200 · DOI
  49. Savina, 2006, NOX2 controls phagosomal pH to regulate antigen processing during crosspresentation by dendritic cells, Cell, 126, 205, 10.1016/j.cell.2006.05.035 · DOI
  50. Chauhan, 2006, Signalling and oxidant adaptation in Candida albicans and Aspergillus fumigatus., Nat. Rev. Microbiol., 4, 435, 10.1038/nrmicro1426 · DOI
  51. Thompson, 1992, Interaction and intracellular killing of Candida albicans blastospores by human polymorphonuclear leucocytes, monocytes and monocyte-derived macrophages in aerobic and anaerobic conditions, Clin. Exp. Immunol., 87, 316, 10.1111/j.1365-2249.1992.tb02994.x · DOI
  52. Azevedo, 2015, A metabolic shift toward pentose phosphate pathway is necessary for amyloid fibril- and phorbol 12-myristate 13-acetate-induced Neutrophil Extracellular Trap (NET) Formation, J. Biol. Chem., 290, 22174, 10.1074/jbc.M115.640094 · DOI
  53. Jawale, 2020, Restoring glucose uptake rescues neutrophil dysfunction and protects against systemic fungal infection in mouse models of kidney disease, Sci. Transl. Med., 12, eaay5691, 10.1126/scitranslmed.aay5691 · DOI
  54. Hara, 2007, The adaptor protein CARD9 is essential for the activation of myeloid cells through ITAM-associated and Toll-like receptors, Nat. Immunol., 8, 619, 10.1038/ni1466 · DOI
  55. Rogers, 2005, Syk-dependent cytokine induction by Dectin-1 reveals a novel pattern recognition pathway for C type lectins, Immunity, 22, 507, 10.1016/j.immuni.2005.03.004 · DOI
  56. Joffre, 2009, Internalization of dectin-1 terminates induction of inflammatory responses, Eur. J. Immunol., 39, 507, 10.1002/eji.200838687 · DOI
  57. Westman, J., Walpole, G.F.W., Kasper, L., Xue, B.Y., Elshafee, O., Hube, B., and Grinstein, S. (2020). Lysosome fusion maintains phagosome integrity during fungal infection. Cell Host Microbe. · DOI
  58. Aybay, 1996, Tumor necrosis factor (TNF) induction from monocyte/macrophages by Candida species, Immunobiology, 196, 363, 10.1016/S0171-2985(96)80059-3 · DOI
  59. Ganesan, 2014, Caspase-8 modulates dectin-1 and complement receptor 3-driven IL-1β production in response to β-glucans and the fungal pathogen, Candida albicans., J. Immunol., 193, 2519, 10.4049/jimmunol.1400276 · DOI
  60. Yamamoto, 1997, Involvement of mannose receptor in cytokine interleukin-1beta (IL-1beta), IL-6, and granulocyte-macrophage colony-stimulating factor responses, but not in chemokine macrophage inflammatory protein 1beta (MIP-1beta), MIP-2, and KC responses, caused by attachment of Candida albicans to macrophages, Infect. Immun., 65, 1077, 10.1128/iai.65.3.1077-1082.1997 · DOI
  61. Chin, 2014, Early expression of local cytokines during systemic Candida albicans infection in a murine intravenous challenge model, Biomed. Rep., 2, 869, 10.3892/br.2014.365 · DOI
  62. Romani, 1997, Initiation of T-helper cell immunity to Candida albicans by IL-12: The role of neutrophils, Chem. Immunol., 68, 110
  63. Maher, 2015, Candida albicans stimulates IL-23 release by human dendritic cells and downstream IL-17 secretion by Vδ1 T cells, J. Immunol., 194, 5953, 10.4049/jimmunol.1403066 · DOI
  64. Mohammadi, 2020, Relationship between antifungal susceptibility profile and virulence factors in Candida albicans isolated from nail specimens, Rev. Soc. Bras. Med. Trop., 53, doi, 10.1590/0037-8682-0214-2019 · DOI
  65. Naglik, 2004, Candida albicans proteinases and host/pathogen interactions, Cell. Microbiol., 6, 915, 10.1111/j.1462-5822.2004.00439.x · DOI
  66. Hu, 2011, Priming microenvironments dictate cytokine requirements for T helper 17 cell lineage commitment, Immunity, 35, 1010, 10.1016/j.immuni.2011.10.013 · DOI
  67. Weindl, 2007, Human epithelial cells establish direct antifungal defense through TLR4-mediated signaling, J. Clin. Investig., 117, 3664
  68. Tomalka, 2015, β-Defensin 1 plays a role in acute mucosal defense against Candida albicans., J. Immunol., 194, 1788, 10.4049/jimmunol.1203239 · DOI
  69. Byrd, 2013, An extracellular matrix-based mechanism of rapid neutrophil extracellular trap formation in response to Candida albicans., J. Immunol., 190, 4136, 10.4049/jimmunol.1202671 · DOI
  70. Gladiator, 2013, Cutting edge: IL-17-secreting innate lymphoid cells are essential for host defense against fungal infection, J. Immunol., 190, 521, 10.4049/jimmunol.1202924 · DOI · Paper page
  71. Bishu, 2014, Rheumatoid arthritis patients exhibit impaired Candida albicans-specific Th17 responses, Arthr. Res. Ther., 16, R50, 10.1186/ar4480 · DOI
  72. Yano, 2010, Epithelial cell-derived S100 calcium-binding proteins as key mediators in the hallmark acute neutrophil response during Candida vaginitis, Infect. Immun., 78, 5126, 10.1128/IAI.00388-10 · DOI
  73. Yano, 2014, Vaginal epithelial cell-derived S100 alarmins induced by Candida albicans via pattern recognition receptor interactions are sufficient but not necessary for the acute neutrophil response during experimental vaginal candidiasis, Infect. Immun., 82, 783, 10.1128/IAI.00861-13 · DOI
  74. Wirnsberger, 2014, Jagunal homolog 1 is a critical regulator of neutrophil function in fungal host defense, Nat. Genet., 46, 1028, 10.1038/ng.3070 · DOI
  75. Willcox, 1998, Interactions between Candida species and platelets, J. Med. Microbiol., 47, 103, 10.1099/00222615-47-2-103 · DOI
  76. Yeaman, 1996, Resistance to platelet microbicidal protein results in increased severity of experimental Candida albicans endocarditis, Infect. Immun., 64, 1379, 10.1128/iai.64.4.1379-1384.1996 · DOI
  77. Alam, 2020, Candida albicans enhances meropenem tolerance of Pseudomonas aeruginosa in a dual-species biofilm, J. Antimicrob. Chemother., 75, 925, 10.1093/jac/dkz514 · DOI
  78. Ambe, 2020, The prevalence, risk factors and antifungal sensitivity pattern of oral candidiasis in HIV/AIDS patients in Kumba District Hospital, South West Region, Cameroon, Pan Afr. Med. J., 36, 23, 10.11604/pamj.2020.36.23.18202 · DOI
  79. Kirti, 2019, Prevalence of oral Candidiasis in Indian HIV sero-positive patients with CD4(+) cell count correlation, Indian J. Otolaryngol. Head Neck Surg. Off. Publ. Assoc. Otolaryngol. India, 71, 124, 10.1007/s12070-018-1342-3 · DOI
  80. Naglik, 2017, Candida albicans-epithelial interactions and induction of mucosal innate immunity, Curr. Opin. Microbiol., 40, 104, 10.1016/j.mib.2017.10.030 · DOI
  81. Nikou, S.A., Kichik, N., Brown, R., Ponde, N.O., Ho, J., Naglik, J.R., and Richardson, J.P. (2019). Candida albicans interactions with mucosal surfaces during health and disease. Pathogens, 8. · DOI · Paper page
  82. Pavlova, A., and Sharafutdinov, I. (2020). Recognition of Candida albicans and role of innate type 17 immunity in oral candidiasis. Microorganisms, 8. · DOI
  83. Richardson, 2019, Candida innate immunity at the mucosa, Semin. Cell Dev. Biol., 89, 58, 10.1016/j.semcdb.2018.02.026 · DOI
  84. Moyes, 2010, A biphasic innate immune MAPK response discriminates between the yeast and hyphal forms of Candida albicans in epithelial cells, Cell Host Microbe, 8, 225, 10.1016/j.chom.2010.08.002 · DOI
  85. Moyes, 2014, Protection against epithelial damage during Candida albicans infection is mediated by PI3K/Akt and mammalian target of rapamycin signaling, J. Infect. Dis., 209, 1816, 10.1093/infdis/jit824 · DOI
  86. Richardson, 2018, Processing of Candida albicans Ece1p Is critical for Candidalysin maturation and fungal virulence, mBio, 9, e02178-17, 10.1128/mBio.02178-17 · DOI
  87. Urban, 2006, Neutrophil extracellular traps capture and kill Candida albicans yeast and hyphal forms, Cell. Microbiol., 8, 668, 10.1111/j.1462-5822.2005.00659.x · DOI
  88. Altmeier, S., Toska, A., Sparber, F., Teijeira, A., Halin, C., and LeibundGut-Landmann, S. (2016). IL-1 coordinates the neutrophil response to C. albicans in the oral mucosa. PLoS Pathog., 12. · DOI · Paper page
  89. Hise, 2009, An essential role for the NLRP3 inflammasome in host defense against the human fungal pathogen Candida albicans., Cell Host Microbe, 5, 487, 10.1016/j.chom.2009.05.002 · DOI
  90. Conti, 2011, New mechanism of oral immunity to mucosal candidiasis in hyper-IgE syndrome, Mucosal Immunol., 4, 448, 10.1038/mi.2011.5 · DOI
  91. Huppler, 2015, Neutrophils do not express IL-17A in the context of acute oropharyngeal Candidiasis, Pathogens, 4, 559, 10.3390/pathogens4030559 · DOI
  92. Liu, 2011, Gain-of-function human STAT1 mutations impair IL-17 immunity and underlie chronic mucocutaneous candidiasis, J. Exp. Med., 208, 1635, 10.1084/jem.20110958 · DOI
  93. Sobel, 1992, Pathogenesis and treatment of recurrent vulvovaginal candidiasis, Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am., 14, S148, 10.1093/clinids/14.Supplement_1.S148 · DOI
  94. Sobel, 1997, Vaginitis, N. Eng. J. Med., 337, 1896, 10.1056/NEJM199712253372607 · DOI
  95. Ferreira, 2016, Vulvovaginal candidiasis: Epidemiology, microbiology and risk factors, Crit. Rev. Microbiol., 42, 905, 10.3109/1040841X.2015.1091805 · DOI · Paper page
  96. Sobel, 2007, Vulvovaginal candidosis, Lancet, 369, 1961, 10.1016/S0140-6736(07)60917-9 · DOI · Paper page
  97. Giraldo, 2007, Mannose-binding lectin gene polymorphism, vulvovaginal candidiasis, and bacterial vaginosis, Obstet. Gynecol., 109, 1123, 10.1097/01.AOG.0000260386.17555.a5 · DOI
  98. Hammad, 2018, Mannose-binding lectin gene polymorphism and its association with susceptibility to recurrent vulvovaginal candidiasis, BioMed. Res. Int., 2018, 7648152, 10.1155/2018/7648152 · DOI
  99. Jaeger, 2016, Association of a variable number tandem repeat in the NLRP3 gene in women with susceptibility to RVVC, Eur. J. Clin. Microbiol. Infect. Dis. Off. Publ. European Soc. Clin. Microbiol., 35, 797, 10.1007/s10096-016-2600-5 · DOI
  100. Rosentul, 2014, Gene polymorphisms in pattern recognition receptors and susceptibility to idiopathic recurrent vulvovaginal candidiasis, Front. Microbiol., 5, 483, 10.3389/fmicb.2014.00483 · DOI
  101. Fidel, 1995, Circulating CD4 and CD8 T cells have little impact on host defense against experimental vaginal candidiasis, Infect. Immun., 63, 2403, 10.1128/iai.63.7.2403-2408.1995 · DOI
  102. Leigh, 2001, Candida-specific systemic cell-mediated immune reactivities in human immunodeficiency virus-positive persons with mucosal candidiasis, J. Infect. Dis., 183, 277, 10.1086/317944 · DOI
  103. White, 1996, Is vulvovaginal candidiasis an AIDS-related illness?, Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am., 22, S124, 10.1093/clinids/22.Supplement_2.S124 · DOI
  104. Graziani, 2018, Candida vaginitis: Virulence, host response and vaccine prospects, Med. Mycol., 56, 26, 10.1093/mmy/myx139 · DOI
  105. Rosati, D., Bruno, M., Jaeger, M., Ten Oever, J., and Netea, M.G. (2020). Recurrent vulvovaginal Candidiasis: An immunological perspective. Microorganisms, 8. · DOI · Paper page
  106. Yano, J., Peters, B.M., Noverr, M.C., and Fidel, P.L. (2018). Novel mechanism behind the immunopathogenesis of vulvovaginal Candidiasis: “Neutrophil Anergy”. Infect. Immun., 86. · DOI
  107. Peters, B.M., Yano, J., Noverr, M.C., and Fidel, P.L. (2014). Candida vaginitis: When opportunism knocks, the host responds. PLoS Pathog., 10. · DOI
  108. Fidel, 2004, An intravaginal live Candida challenge in humans leads to new hypotheses for the immunopathogenesis of vulvovaginal candidiasis, Infect. Immun., 72, 2939, 10.1128/IAI.72.5.2939-2946.2004 · DOI
  109. Nomanbhoy, 2002, Vaginal and oral epithelial cell anti-Candida activity, Infect. Immun., 70, 7081, 10.1128/IAI.70.12.7081-7088.2002 · DOI
  110. Soloviev, 2011, Regulation of innate immune response to Candida albicans infections by αMβ2-Pra1p interaction, Infect. Immun., 79, 1546, 10.1128/IAI.00650-10 · DOI
  111. Yano, J., Noverr, M.C., and Fidel, P.L. (2017). Vaginal heparan sulfate linked to neutrophil dysfunction in the acute inflammatory response associated with experimental vulvovaginal Candidiasis. mBio, 8. · DOI
  112. Hayashi, 1988, Hormonal modification of epithelial differentiation and expression of cell surface heparan sulfate proteoglycan in the mouse vaginal epithelium. An immunohistochemical and electron microscopic study, Lab. Investig. J. Tech. Methods Pathol., 58, 68
  113. Hopke, 2018, Dynamic fungal cell wall architecture in stress adaptation and immune evasion, Trends Microbiol., 26, 284, 10.1016/j.tim.2018.01.007 · DOI
  114. Ballou, 2016, Lactate signalling regulates fungal β-glucan masking and immune evasion, Nat. Microbiol., 2, 16238, 10.1038/nmicrobiol.2016.238 · DOI · Paper page
  115. Ene, 2013, Growth of Candida albicans cells on the physiologically relevant carbon source lactate affects their recognition and phagocytosis by immune cells, Infect. Immun., 81, 238, 10.1128/IAI.01092-12 · DOI
  116. Cottier, F., Sherrington, S., Cockerill, S., Del Olmo Toledo, V., Kissane, S., Tournu, H., Orsini, L., Palmer, G.E., Pérez, J.C., and Hall, R.A. (2019). Remasking of Candida albicans β-glucan in response to environmental pH is regulated by quorum sensing. mBio, 10. · DOI
  117. Pericolini, E., Perito, S., Castagnoli, A., Gabrielli, E., Mencacci, A., Blasi, E., Vecchiarelli, A., and Wheeler, R.T. (2018). Epitope unmasking in vulvovaginal candidiasis is associated with hyphal growth and neutrophilic infiltration. PLoS ONE, 13. · DOI
  118. Spellberg, 2005, Mice with disseminated candidiasis die of progressive sepsis, J. Infect. Dis., 192, 336, 10.1086/430952 · DOI · Paper page
  119. Swamydas, 2016, CXCR1-mediated neutrophil degranulation and fungal killing promote Candida clearance and host survival, Sci. Transl. Med., 8, 322ra310, 10.1126/scitranslmed.aac7718 · DOI
  120. Jenne, 2015, Platelets in inflammation and infection, Platelets, 26, 286, 10.3109/09537104.2015.1010441 · DOI
  121. Arman, 2014, Amplification of bacteria-induced platelet activation is triggered by FcγRIIA, integrin αIIbβ3, and platelet factor 4, Blood, 123, 3166, 10.1182/blood-2013-11-540526 · DOI
  122. Seyoum, 2018, Human blood platelets and viruses: Defense mechanism and role in the removal of viral pathogens, Thromb. J., 16, 16, 10.1186/s12959-018-0170-8 · DOI
  123. Ghuman, 2019, Mucor circinelloides induces platelet aggregation through integrin αIIbβ3 and FcγRIIA, Platelets, 30, 256, 10.1080/09537104.2017.1420152 · DOI
  124. Eberl, 2019, Candida: Platelet interaction and platelet activity in vitro, J. Innate Immun., 11, 52, 10.1159/000491030 · DOI
  125. Watson, 2016, Human platelet activation by Escherichia coli: Roles for FcγRIIA and integrin αIIbβ3, Platelets, 27, 535, 10.3109/09537104.2016.1148129 · DOI
  126. Bertling, 2010, Candida albicans and its metabolite gliotoxin inhibit platelet function via interaction with thiols, Thromb. Haemost., 104, 270, 10.1160/TH09-11-0769 · DOI
  127. Kupfahl, 2007, Candida species fail to produce the immunosuppressive secondary metabolite gliotoxin in vitro, FEMS Yeast Res., 7, 986, 10.1111/j.1567-1364.2007.00256.x · DOI
  128. Grubb, 2008, Candida albicans-endothelial cell interactions: A key step in the pathogenesis of systemic candidiasis, Infect. Immun., 76, 4370, 10.1128/IAI.00332-08 · DOI · Paper page
  129. Phan, 2005, N-cadherin mediates endocytosis of Candida albicans by endothelial cells, J. Biol. Chem., 280, 10455, 10.1074/jbc.M412592200 · DOI · Paper page
  130. Shintaku, 2013, Human endothelial cells internalize Candida parapsilosis via N-WASP-mediated endocytosis, Infect. Immun., 81, 2777, 10.1128/IAI.00535-13 · DOI
  131. Gazendam, 2014, Two independent killing mechanisms of Candida albicans by human neutrophils: Evidence from innate immunity defects, Blood, 124, 590, 10.1182/blood-2014-01-551473 · DOI

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Metadata

Authors
Bojang, E., Ghuman, H., Kumwenda, P., & Hall, R. A.
Venue
Journal of Fungi
Publisher
MDPI AG
Published
2021-02-06
Volume
7
Issue
2
Pages
119
ISSN
2309-608X
DOI
10.3390/jof7020119
Cited by
96
References
13
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • Medical Research Council (MR/N013913/1)
  • Wellcome Trust (097377/Z/11/Z)
  • Biotechnology and Biological Sciences Research Council (BB/R00966X/1)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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