Dear Colleagues,

Fungi are the third most abundant life form on Earth and evolving environmental changes could provide the selective advantage for some of these species to emerge as pathogens. This potential is compounded by increased application of suppressive immunotherapies, where populations of immune suppressed recipients are placed at increased risk. In this respect, there are 148,000 identified species of fungi, and likely many more that are undiscovered. Suffice it to say that environmental change may select and spread a new collection of these as dominant fungal pathogens. As encounters with potential fungal pathogens increases, it is then a matter of coincidental inoculation among permissive immune-deficient hosts. Gathering knowledge of immune recognition and effector function in known fungal infections provides valuable insight for understanding these emerging fungal diseases.

As with other microbes, resistance to fungal infection in healthy mammalian hosts is initiated by sensing simple molecular fingerprints know as pathogen associated molecular pattern (PAMPs). Conserved fungal PAMPs initiate innate immune responses via pattern recognition receptors (PRRs), also a characterized as a phylogenetically conserved system for mounting resistance to microbial invaders. Research has shown us that some fungi possess mechanisms of resistance/virulence allowing them to minimize or avoid this detection system while others block immune effector functions and persist in the host. Enhancing essential anti-fungal responses by restoring or replacing dysfunctional innate recognition might offer a means of enhanced protection in certain susceptible populations.

In a broader sense, innate immunity needed for resisting infection, including fungi, uses an integrated system comprised of innate tissue barriers (e.g., skin), inflammation, phagocytes, opsonization and T cell immunity to provide comprehensive resistance and effective clearance. An indispensable cog for resisting systemic infections are phagocytes. Depending upon the location of the infection and the fungal species involved, neutrophils can display effective fungal resistance traits (e.g., Candida and Cryptococcus), but against other fungi neutrophils can be less than adequate (e.g., Histoplasma). Alternatively, T cell dependent macrophage activation may serve as the more protective effector mechanism. Indeed, fungal pathogenic adaptation can include phenotypic changes manifested during fungal infection as a mechanism that limits phagocytic clearance. Furthermore, the neutrophil’s capacity to eliminate invading fungal cells can be seriously limited by clinical interventions such as stress, bone marrow ablation, cytoreductive cancer treatment and long-term cortical steroid therapy. Moreover, advancing our understanding of the limits in altered host resistance can provide insight into the potential for new pathogenic niches and perhaps targeted treatments that address these dynamic changes in fungal distribution.

Dr. Ron Garner
Dr. Eleonora Dubljanin
Guest Editors

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• fungi
• fungal pathogens
• fungal infection
• host response
• innate immunity
• Candida
• Cryptococcus
• Histoplasma

• Pneumocystis

• Mucor
• Aspergillus
• emerging opportunistic fungal pathogens