Immune Recognition of Candida albicans ß-glucan by Dectin-1

Neil A. R. Gow, Mihai G. Netea, Carol A. Munro, Gerben Ferwerda, Steven Bates, Héctor M. Mora-Montes, Louise Walker, Trees Jansen, Liesbeth Jacobs, Vicky Tsoni, Gordon D. Brown, Frank C. Odds, Jos W. M. Van der Meer, Alistair J. P. Brown, Bart Jan Kullberg

Research output: Contribution to journalArticle

172 Citations (Scopus)

Abstract

Beta (1,3)-glucans represent 40% of the cell wall of the yeast Candida albicans. The dectin-1 lectin-like receptor has shown to recognize fungal beta (1,3)-glucans and induce innate immune responses. The importance of beta-glucan-dectin-1 pathways for the recognition of C. albicans by human primary blood cells has not been firmly established. In this study we demonstrate that cytokine production by both human peripheral blood mononuclear cells and murine macrophages is dependent on the recognition of beta-glucans by dectin-1. Heat killing of C. albicans resulted in exposure of beta-glucans on the surface of the cell wall and subsequent recognition by dectin-1, whereas live yeasts stimulated monocytes mainly via recognition of cell-surface mannans. Dectin-1 induced cytokine production through the following 2 pathways: Syk-dependent production of the T-helper (Th) 2-type anti-inflammatory cytokine interleukin-10 and Toll-like receptor-Myd88-dependent stimulation of monocyte-derived proinflammatory cytokines, such as tumor necrosis factor-alpha . In contrast, stimulation of Th1-type cytokines, such as interferon-gamma , by C. albicans was independent of the recognition of beta-glucans by dectin-1. In conclusion, C. albicans induces production of monocyte-derived and T cell-derived cytokines through distinct pathways dependent on or independent of dectin-1.
Original languageEnglish
Pages (from-to)1565-1571
Number of pages7
JournalThe journal of infectious diseases
Volume196
Issue number10
DOIs
Publication statusPublished - 15 Nov 2007

Keywords

  • animals
  • candida albicans
  • candidiasis
  • disease models, animal
  • humans
  • leukocytes, mononuclear
  • macrophages, peritoneal
  • membrane proteins
  • mice
  • mice, knockout
  • nerve tissue proteins
  • receptors, immunologic

Cite this

Gow, N. A. R., Netea, M. G., Munro, C. A., Ferwerda, G., Bates, S., Mora-Montes, H. M., ... Kullberg, B. J. (2007). Immune Recognition of Candida albicans ß-glucan by Dectin-1. The journal of infectious diseases, 196(10), 1565-1571. https://doi.org/10.1086/523110

Immune Recognition of Candida albicans ß-glucan by Dectin-1. / Gow, Neil A. R.; Netea, Mihai G.; Munro, Carol A.; Ferwerda, Gerben; Bates, Steven; Mora-Montes, Héctor M.; Walker, Louise; Jansen, Trees; Jacobs, Liesbeth; Tsoni, Vicky; Brown, Gordon D.; Odds, Frank C.; Van der Meer, Jos W. M.; Brown, Alistair J. P.; Kullberg, Bart Jan.

In: The journal of infectious diseases, Vol. 196, No. 10, 15.11.2007, p. 1565-1571.

Research output: Contribution to journalArticle

Gow, NAR, Netea, MG, Munro, CA, Ferwerda, G, Bates, S, Mora-Montes, HM, Walker, L, Jansen, T, Jacobs, L, Tsoni, V, Brown, GD, Odds, FC, Van der Meer, JWM, Brown, AJP & Kullberg, BJ 2007, 'Immune Recognition of Candida albicans ß-glucan by Dectin-1', The journal of infectious diseases, vol. 196, no. 10, pp. 1565-1571. https://doi.org/10.1086/523110
Gow, Neil A. R. ; Netea, Mihai G. ; Munro, Carol A. ; Ferwerda, Gerben ; Bates, Steven ; Mora-Montes, Héctor M. ; Walker, Louise ; Jansen, Trees ; Jacobs, Liesbeth ; Tsoni, Vicky ; Brown, Gordon D. ; Odds, Frank C. ; Van der Meer, Jos W. M. ; Brown, Alistair J. P. ; Kullberg, Bart Jan. / Immune Recognition of Candida albicans ß-glucan by Dectin-1. In: The journal of infectious diseases. 2007 ; Vol. 196, No. 10. pp. 1565-1571.
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abstract = "Beta (1,3)-glucans represent 40{\%} of the cell wall of the yeast Candida albicans. The dectin-1 lectin-like receptor has shown to recognize fungal beta (1,3)-glucans and induce innate immune responses. The importance of beta-glucan-dectin-1 pathways for the recognition of C. albicans by human primary blood cells has not been firmly established. In this study we demonstrate that cytokine production by both human peripheral blood mononuclear cells and murine macrophages is dependent on the recognition of beta-glucans by dectin-1. Heat killing of C. albicans resulted in exposure of beta-glucans on the surface of the cell wall and subsequent recognition by dectin-1, whereas live yeasts stimulated monocytes mainly via recognition of cell-surface mannans. Dectin-1 induced cytokine production through the following 2 pathways: Syk-dependent production of the T-helper (Th) 2-type anti-inflammatory cytokine interleukin-10 and Toll-like receptor-Myd88-dependent stimulation of monocyte-derived proinflammatory cytokines, such as tumor necrosis factor-alpha . In contrast, stimulation of Th1-type cytokines, such as interferon-gamma , by C. albicans was independent of the recognition of beta-glucans by dectin-1. In conclusion, C. albicans induces production of monocyte-derived and T cell-derived cytokines through distinct pathways dependent on or independent of dectin-1.",
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AU - Ferwerda, Gerben

AU - Bates, Steven

AU - Mora-Montes, Héctor M.

AU - Walker, Louise

AU - Jansen, Trees

AU - Jacobs, Liesbeth

AU - Tsoni, Vicky

AU - Brown, Gordon D.

AU - Odds, Frank C.

AU - Van der Meer, Jos W. M.

AU - Brown, Alistair J. P.

AU - Kullberg, Bart Jan

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N2 - Beta (1,3)-glucans represent 40% of the cell wall of the yeast Candida albicans. The dectin-1 lectin-like receptor has shown to recognize fungal beta (1,3)-glucans and induce innate immune responses. The importance of beta-glucan-dectin-1 pathways for the recognition of C. albicans by human primary blood cells has not been firmly established. In this study we demonstrate that cytokine production by both human peripheral blood mononuclear cells and murine macrophages is dependent on the recognition of beta-glucans by dectin-1. Heat killing of C. albicans resulted in exposure of beta-glucans on the surface of the cell wall and subsequent recognition by dectin-1, whereas live yeasts stimulated monocytes mainly via recognition of cell-surface mannans. Dectin-1 induced cytokine production through the following 2 pathways: Syk-dependent production of the T-helper (Th) 2-type anti-inflammatory cytokine interleukin-10 and Toll-like receptor-Myd88-dependent stimulation of monocyte-derived proinflammatory cytokines, such as tumor necrosis factor-alpha . In contrast, stimulation of Th1-type cytokines, such as interferon-gamma , by C. albicans was independent of the recognition of beta-glucans by dectin-1. In conclusion, C. albicans induces production of monocyte-derived and T cell-derived cytokines through distinct pathways dependent on or independent of dectin-1.

AB - Beta (1,3)-glucans represent 40% of the cell wall of the yeast Candida albicans. The dectin-1 lectin-like receptor has shown to recognize fungal beta (1,3)-glucans and induce innate immune responses. The importance of beta-glucan-dectin-1 pathways for the recognition of C. albicans by human primary blood cells has not been firmly established. In this study we demonstrate that cytokine production by both human peripheral blood mononuclear cells and murine macrophages is dependent on the recognition of beta-glucans by dectin-1. Heat killing of C. albicans resulted in exposure of beta-glucans on the surface of the cell wall and subsequent recognition by dectin-1, whereas live yeasts stimulated monocytes mainly via recognition of cell-surface mannans. Dectin-1 induced cytokine production through the following 2 pathways: Syk-dependent production of the T-helper (Th) 2-type anti-inflammatory cytokine interleukin-10 and Toll-like receptor-Myd88-dependent stimulation of monocyte-derived proinflammatory cytokines, such as tumor necrosis factor-alpha . In contrast, stimulation of Th1-type cytokines, such as interferon-gamma , by C. albicans was independent of the recognition of beta-glucans by dectin-1. In conclusion, C. albicans induces production of monocyte-derived and T cell-derived cytokines through distinct pathways dependent on or independent of dectin-1.

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KW - nerve tissue proteins

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