The human mycobiome in health and disease

Abstract

The mycobiome, referring primarily to the fungal biota in an environment, is an important component of the human microbiome. Despite its importance, it has remained understudied. New culture-independent approaches to determine microbial diversity, such as next-generation sequencing methods, are greatly broadening our view of fungal importance. An integrative analysis of current studies shows that different body sites harbor specific fungal populations, and that diverse mycobiome patterns are associated with various diseases. By interfacing with other biomes, as well as with the host, the mycobiome probably contributes to the progression of fungus-associated diseases and plays an important role in health and disease.

Figure 1

Schematic representation of the fungal ribosomal gene cluster, with binding locations of PCR primers. Within the fungal rDNA, 18S, 5.8S and 28S are separated by ITS1 and ITS2. Several primer sets that target specific regions of the fungal rDNA have been designed and used in previous studies.

Figure 2

Distribution of fungal genera in different body sites. Fungal distributions differ significantly among distant body sites, whereas similar patterns are found in nearby sites. For example, Cladosporium spp., Aspergillus spp., and Penecillium spp. all dominate other fungal genera in both oral and nasal cavities.

Figure 3

Host and environmental factors that contribute to diversity observed in the human mycobiome.

Figure 4

Interaction between the mycobiome and the immune system. Several pattern recognition receptors (PRRs) on phagocytes specifically recognize the pathogen-associated molecular patterns (PAMPs) of fungi. Following this pattern recognition, macrophage and dendritic cells mature and activate T cells through an antigen-presenting process. Activated T cells differentiate into either Th-1, which promotes the phagocytosis of fungi, or Th-2, which activates B cells to release fungi-specific antibodies, depending by which cytokines they are stimulated. IFN, interferon; IL, interleukin; TNF, tumor necrosis factor. (Figure design inspired by the information reported in [16] and [53].)