Research Article: Gut mycobiota dysbiosis and an emergent state of “co-dysbiosis” are associated with IgE sensitization in children with comorbid allergic rhinitis and constipation
Abstract:
The comorbidity of allergic rhinitis (AR) and functional constipation (FC), termed ARFC, implies shared gut–immune pathways. Although bacterial dysbiosis has been implicated, the role of the gut mycobiota (fungal community) in this specific comorbidity remains unexplored.
This pilot case-control study characterized the gut mycobiota in 19 ARFC and 17 healthy control (HC) children aged 3–6 years using metagenomic sequencing. Fungal community structure, taxonomic composition, and correlations with IgE levels were analyzed. Cross-kingdom bacterial–fungal interaction networks were constructed, and functional potential was predicted.
Alpha diversity was comparable, whereas beta diversity revealed significant structural shifts in the ARFC gut mycobiota. Key immunomodulatory fungi, including Cenococcum, Dentiscutata, Ambispora, and Saccharomyces, were markedly depleted in ARFC. These taxa served as top discriminators in random forest models and exhibited significant inverse correlations with total and allergen-specific IgE levels. Cross-kingdom network analysis identified dramatic ecological restructuring: the HC network was characterized by prevalent competitive interactions, whereas the ARFC network shifted exclusively to positive correlations, a state termed “co-dysbiosis.” No significant differences were observed in predicted KEGG functional pathways.
This study provides the first evidence that gut mycobiota dysbiosis—marked by depletion of immunoregulatory fungi and an ecological shift toward cooperative interkingdom interactions (“co-dysbiosis”)—is associated with IgE sensitization in ARFC children. These findings position the gut mycobiota as a novel element of the gut–nose axis in allergic disease, warranting further investigation.
Introduction:
The comorbidity of allergic rhinitis (AR) and functional constipation (FC), termed ARFC, implies shared gut–immune pathways. Although bacterial dysbiosis has been implicated, the role of the gut mycobiota (fungal community) in this specific comorbidity remains unexplored.
Read more