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The role of the cell wall in fungal pathogenesis.

Arana DM, Prieto D, Román E, Nombela C, Alonso-Monge R, Pla J - Microb Biotechnol (2008)

Bottom Line: Specific components of the cell wall (called PAMPs) interact with specific receptors in the immune cell (called PRRs), triggering responses whose molecular mechanisms are being elucidated.We review here the main structural carbohydrate components of the fungal wall (glucan, mannan and chitin), how their biogenesis takes place in fungi and the specific receptors that they interact with.Different model fungal pathogens are chosen to illustrate the functional consequences of this interaction.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Microbiología II, Facultad de Farmacia, Universidad Complutense de Madrid, Plaza de Ramón y Cajal s/n, E-28040 Madrid, Spain.

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Related in: MedlinePlus

Activation of the complement system via MBL. The figure shows the activation of the complement cascade in response to fungal mannan recognition mediated by MBL. MBL, mannan‐binding lectin; MAC, membrane attack complex.
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f4: Activation of the complement system via MBL. The figure shows the activation of the complement cascade in response to fungal mannan recognition mediated by MBL. MBL, mannan‐binding lectin; MAC, membrane attack complex.

Mentions: Candida albicans mannan is also recognized by other proteins, called collectins, which are all secreted as large multimeric complexes. At least three collectins, mannose‐binding lectin (MBL), surfactant protein A (SP‐A) and surfactant protein D (SP‐D), have been implicated in antifungal immunity. Mannose‐binding lectin is a serum protein that recognizes selected terminal monosaccharides, such as mannose, fucose and N‐acetylglucosamine (Turner and Hamvas, 2000). Fungal binding by MBL triggers a protease cascade through the MBL‐associated serine proteases (MASP‐1 and MASP‐2) that leads to activation of the complement pathway and deposition (or opsonization) of complement components, such as C3b, on the microbial surface, thereby promoting opsonic fungal recognition (Kilpatrick, 2002; Holmskov et al., 2003) (Fig. 4). MBL plays an important role in the first‐line defence against C. albicans without the need for opsonophagocytosis by DCs, in which a direct interaction of MBL with C. albicans results in agglutination and accelerated complement activation via the lectin pathway, leading to inhibition of growth (Ip and Lau, 2004). However, a recent work indicates that the lectin pathway of complement activation in human neutrophils is important for the opsonophagocytosis of yeasts but not of bacteria (Brouwer et al., 2008). SP‐A and SP‐D recognize a broad range of microbes, including H. capsulatum, A. fumigatus, C. albicans and C. neoformans (Kishore et al., 2006), but they do not trigger complement activation and their primary role appears to involve microbial agglutination.


The role of the cell wall in fungal pathogenesis.

Arana DM, Prieto D, Román E, Nombela C, Alonso-Monge R, Pla J - Microb Biotechnol (2008)

Activation of the complement system via MBL. The figure shows the activation of the complement cascade in response to fungal mannan recognition mediated by MBL. MBL, mannan‐binding lectin; MAC, membrane attack complex.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3815752&req=5

f4: Activation of the complement system via MBL. The figure shows the activation of the complement cascade in response to fungal mannan recognition mediated by MBL. MBL, mannan‐binding lectin; MAC, membrane attack complex.
Mentions: Candida albicans mannan is also recognized by other proteins, called collectins, which are all secreted as large multimeric complexes. At least three collectins, mannose‐binding lectin (MBL), surfactant protein A (SP‐A) and surfactant protein D (SP‐D), have been implicated in antifungal immunity. Mannose‐binding lectin is a serum protein that recognizes selected terminal monosaccharides, such as mannose, fucose and N‐acetylglucosamine (Turner and Hamvas, 2000). Fungal binding by MBL triggers a protease cascade through the MBL‐associated serine proteases (MASP‐1 and MASP‐2) that leads to activation of the complement pathway and deposition (or opsonization) of complement components, such as C3b, on the microbial surface, thereby promoting opsonic fungal recognition (Kilpatrick, 2002; Holmskov et al., 2003) (Fig. 4). MBL plays an important role in the first‐line defence against C. albicans without the need for opsonophagocytosis by DCs, in which a direct interaction of MBL with C. albicans results in agglutination and accelerated complement activation via the lectin pathway, leading to inhibition of growth (Ip and Lau, 2004). However, a recent work indicates that the lectin pathway of complement activation in human neutrophils is important for the opsonophagocytosis of yeasts but not of bacteria (Brouwer et al., 2008). SP‐A and SP‐D recognize a broad range of microbes, including H. capsulatum, A. fumigatus, C. albicans and C. neoformans (Kishore et al., 2006), but they do not trigger complement activation and their primary role appears to involve microbial agglutination.

Bottom Line: Specific components of the cell wall (called PAMPs) interact with specific receptors in the immune cell (called PRRs), triggering responses whose molecular mechanisms are being elucidated.We review here the main structural carbohydrate components of the fungal wall (glucan, mannan and chitin), how their biogenesis takes place in fungi and the specific receptors that they interact with.Different model fungal pathogens are chosen to illustrate the functional consequences of this interaction.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Microbiología II, Facultad de Farmacia, Universidad Complutense de Madrid, Plaza de Ramón y Cajal s/n, E-28040 Madrid, Spain.

Show MeSH
Related in: MedlinePlus