Abstract
The gut microbiome consists of a multi-kingdom microbial community. Whilst the role of bacteria as causal contributors governing host physiological development is well established, the role of fungi remains to be determined. Here, we use germ-free mice colonized with defined species of bacteria, fungi, or both to differentiate the causal role of fungi on microbiome assembly, immune development, susceptibility to colitis, and airway inflammation. Fungal colonization promotes major shifts in bacterial microbiome ecology, and has an independent effect on innate and adaptive immune development in young mice. While exclusive fungal colonization is insufficient to elicit overt dextran sulfate sodium-induced colitis, bacterial and fungal co-colonization increase colonic inflammation. Ovalbumin-induced airway inflammation reveals that bacterial, but not fungal colonization is necessary to decrease airway inflammation, yet fungi selectively promotes macrophage infiltration in the airway. Together, our findings demonstrate a causal role for fungi in microbial ecology and host immune functionality, and therefore prompt the inclusion of fungi in therapeutic approaches aimed at modulating early life microbiomes.
Highlights
The gut microbiome consists of a multi-kingdom microbial community
We utilized the Oligo-MM12 consortium, which consists of 12 mouse-derived bacterial species that are persistent, inheritable, and eliciting of immune responses in mice that are similar to a complex microbiota[27,28]
Bacteria were only detected in B and bacteria and yeasts (BY) mice, while fungi were detected in Y and BY groups (Fig. 1b–e)
Summary
The gut microbiome consists of a multi-kingdom microbial community. Whilst the role of bacteria as causal contributors governing host physiological development is well established, the role of fungi remains to be determined. We use germ-free mice colonized with defined species of bacteria, fungi, or both to differentiate the causal role of fungi on microbiome assembly, immune development, susceptibility to colitis, and airway inflammation. Our findings demonstrate a causal role for fungi in microbial ecology and host immune functionality, and prompt the inclusion of fungi in therapeutic approaches aimed at modulating early life microbiomes. Prospective populationlevel studies have associated microbiome alterations with dysregulation of host physiology and increased susceptibility to immune, metabolic, neurological, and psychiatric diseases[8,9]. These studies have been mainly focused on bacteria, without accounting for the multi-kingdom and multitrophic nature of this microbial ecosystem[10]. Gut bacterial and fungal communities inhabit similar intestinal habitats[15], and fungal-bacterial correlations have been identified in human cohort studies[12,13], suggesting integral ecological interactions during early stages of colonization[7]
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