• Mycobiome in health and disease
  • Roozbeh Yalfani,1,*
    1. Department of Nursing, Faculty of Medical Sciences, Islamic Azad University,Varamin-Pishva branch, Tehran, Iran


  • Introduction: Human body is a reservoir of a large number of microorganisms, their genomes, enzymes, and metabolites clubbed together and referred to as "Microbiome", which is further housed in various human organs. The microbiome is the collection of bacteria, viruses, fungi, and other microorganisms that live in and on all mammalian organisms. The ratio of this community of microorganisms to normal cells in the body is about 1.3 to 1.69. A large number of diseases arise from a dysfunctional microbiome. The microbiome has varying effects on the immune response. A few conditions that the microbiome has been associated with are inflammatory bowel disease (IBD), type 1 diabetes, multiple sclerosis, HIV, and even some cancers. The overarching term for microbiota imbalance is dysbiosis, or loss of beneficial microbiota, overgrowth of harmful microorganisms, and/or loss of microbial diversity. Dysbiosis can occur from overuse of antibiotics, an unhealthy lifestyle, recurrent or serious infections, and the like. Fecal microbiota transplantation (FMT) has been used as a treatment for CDI, a major nosocomial diarrheal infection that is often recurrent and represents a large clinical burden in healthcare. CDI is now widely recognized as being related to an imbalance in the microbiome of the gut and, as such, is a target for microbiota-based therapies. FMT is the transfer of fecal material from a healthy patient to a patient in a state of gut dysbiosis.
  • Methods: FMT delivered by colonoscopy has been highly effective in the treatment and staving off of CDI. It has been shown to decrease proinflammatory cytokines such as IL-6 and TNF-α and increase anti-inflammatory bacteria like Lactobacillaceae and Ruminococcaceae, thus restoring microbiota balance in the recipient. Mycobiome (first voiced in 2009) "the fungal population" acquires only 0.1% of the total microbiome — counterbalance the number of bacterial species by being larger in size. Amongst the microorganisms that colonize the GI tract, fungi are much less abundant than bacteria, with recent estimates suggesting that fungi make up 1–3% of the total microbes in human feces. Despite their modest input to the biomass of the gut microbiota, fungal colonizers make important contributions to the development and regulation of local and systemic immune responses in the host early in life. Similar to other body sites, the gut mycobiome starts developing from birth, as fungi have been detected in the gut of neonates as early as one day after delivery.
  • Results: Analysis of the fungal ecology of paired samples between mothers and neonates supports vertical transmission as an ecological mechanism for the establishment of the neonatal mycobiome.An additional maternally derived source of fungal exposure in early life is breast milk. Analysis of the fungal constituents in breast milk revealed the presence of Candida, Alternaria, Rhodotorula, Malassezia, Davidiella, Sistotrema, and Penicillium, all of which are known to colonize the intestinal tract. Beyond maternally derived factors, the early-life mycobiome is influenced by a variety of host-intrinsic (e.g., genetics, sex, and age) and extrinsic (e.g., drugs, food, and hygiene) factors during infancy. As with the bacterial microbiome, mycobiome-immune interactions in the gut are bidirectional. The mycobiome is shaped by selective pressure from mucosal immunoglobulins. Secretory IgA produced in response to intestinal colonization by C. albicans is preferentially directed against the hyphal morphotype, producing a negative selective pressure that favors colonization by the yeast form. Mucosal phagocytes also contribute to shaping the mycobiome through recognition of intestinal fungi and regulation of antifungal humoral responses.
  • Conclusion: Mycobiome perturbations can constitute dysbiotic states resulting in pathological mucosal immune responses. Mechanistically, this is perhaps best exemplified by the consequences of antibiotic-induced dysbiosis for Candida-immune interactions. By disrupting homeostatic transkingdom interactions between commensal bacteria and Candida, antibiotic treatment enables hyphal morphogenesis. Hyphal Candida expresses adhesins and other virulence factors that induce epithelial damage, barrier disruption, immune activation, production of pro-inflammatory cytokines, and the recruitment of inflammatory cells. Fungal infection and epithelial cell activation/damage can release alarmins, which further activate antigen presenting cells and exacerbate innate and adaptive immune responses. Mycobiome dysbiosis may also contribute to IBD pathogenesis in humans. Increased absolute abundance of C. albicans has been associated with IBD flares, and its relative abundance is also predictive of clinical remission after fecal microbiota transfer (FMT) treatment, which led to decreased Candida sp. abundance. This work revealed the role of mycobiome dysbiosis in chronic colitis development and resolution, likely through a combination of immune and ecological mechanisms.
  • Keywords: Human microbiome, Microbiome-host interactions, Mycobiome, Immune Response