Chapter 13 : Overview of Fungal Pathogens

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This chapter on fungal pathogens focuses on the most prominent group of fungi that cause life-threatening diseases, the species and species. The frequency of invasive mycoses due to opportunistic fungal pathogens has increased significantly over the past 2 decades. Infections with fungal pathogens have emerged as an increasing risk faced by patients under continuous immuno-suppression. Macrophages and neutrophilic granulocytes play a major role in killing fungal pathogens like and conidia. Multiple host innate immune and pattern recognition receptors recognize fungal pathogens such as , , and . Galactin-3 is an important pattern recognition receptor that binds pathogen-specific oligosaccharides, delivers antimicrobial activity, and directs fungicidal activity to opportunistic fungal pathogens. Both SCARF1 and CD36 define an evolutionarily conserved pathway for the innate sensing of fungal pathogens. Human pathogenic fungi like secrete proteases such as aspartyl proteases, which assist and direct immune evasion. The understanding of the multiple layers of host immune defense against fungal pathogens has substantially increased during the last years. T cells and antigen-mediated response are important for defense against fungal pathogens. A large number of host pattern recognition molecules have been identified which sense fungal pathogens and at the same time multiple fungal proteins that bind and block host immune attack. The new concept of a virulence repertoire versus single virulence determinants that is currently emerging indicates the complexity of the interaction and the multiple reactions occurring at the pathogen host interface.

Citation: Brakhage A, Zipfel P. 2011. Overview of Fungal Pathogens, p 165-172. In Kaufmann S, Rouse B, Sacks D (ed), The Immune Response to Infection. ASM Press, Washington, DC. doi: 10.1128/9781555816872.ch13
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Immune escape strategies used by human pathogenic fungi. Human pathogenic fungi use similar and related immune escape strategies as shown here for Human pathogenic fungi produce surface proteins that bind host plasma proteins such as plasminogen, complement Factor H, and Factor H like protein (FHL-1). Attached to the fungal surface, host plasminogen can be activated to the active protease that degrades IgG and ECM components. In addition, attached host complement regulators Factor H and FHL-1 control surface opsonization with C3 activation products, thereby resisting phagocytosis and cell lysis. Moreover, human pathogenic fungi secrete proteases like SAPs (secreted aspartyl proteases), which degrade host immune effector proteins and thus aid in immune evasion. The thick cell wall provides an additional mechanical shield, which protects the vulnerable fungal membrane from activated host immune effector compounds.

Citation: Brakhage A, Zipfel P. 2011. Overview of Fungal Pathogens, p 165-172. In Kaufmann S, Rouse B, Sacks D (ed), The Immune Response to Infection. ASM Press, Washington, DC. doi: 10.1128/9781555816872.ch13
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species isolated during invasive candidosis in Europe

Citation: Brakhage A, Zipfel P. 2011. Overview of Fungal Pathogens, p 165-172. In Kaufmann S, Rouse B, Sacks D (ed), The Immune Response to Infection. ASM Press, Washington, DC. doi: 10.1128/9781555816872.ch13
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Pattern recognition receptors on the surface of human phagoycytic cells reacting with fungal cell wall components

Citation: Brakhage A, Zipfel P. 2011. Overview of Fungal Pathogens, p 165-172. In Kaufmann S, Rouse B, Sacks D (ed), The Immune Response to Infection. ASM Press, Washington, DC. doi: 10.1128/9781555816872.ch13

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