Microbiota signatures and genetic risk in pediatric celiac disease

Table 3 Fungal taxa alterations and their pathophysiological implications in celiac disease

Fungal taxon/group	Reported change	Context/condition	Sample type	Possible functional consequence	Nature of evidence
Candida spp./C. albicans	Increase	Pediatric CD; potential immune cross-reactivity	Stool; duodenal biopsy in some studies	Molecular mimicry via hyphal wall protein 1; possible gliadin cross-reactivity and immune activation	Clinical observation + mechanistic hypothesis
Saccharomyces cerevisiae	Increase/variable	Fungal dysbiosis; inflammation-associated context	Mostly stool	ASCA-related immune response; marker of intestinal fungal dysbiosis	Clinical observation + immunological association
Tricholomataceae	Increase	Pediatric CD-associated fungal signature	Fecal samples	Possible marker of altered fungal community structure	Study-dependent clinical observation
Saccharomycetaceae	Increase	Family-level fungal shift in CD	Mostly stool	Fungal ecosystem imbalance; possible dysbiosis marker	Clinical observation + ecological interpretation
Pichia kudriavzevii	Decrease	Loss of commensal fungal diversity	Mostly stool	Reduced protective microbial competition; weakened fungal ecosystem balance	Limited clinical observation + ecological interpretation
Pneumocystis jirovecii	Decrease	Duodenal mucosal fungal profile	Duodenal biopsy	Possible altered mucosal fungal niche; unclear functional relevance	Study-dependent mucosal finding
Fungal community overall	Altered/variable	Active CD, at-risk siblings, and preclinical context	Stool; duodenal biopsy in some studies	Barrier regulation, antigenic environment, T-cell polarization, and immune tolerance	Clinical cohort findings + mechanistic support

CD: Celiac disease; ASCA: Anti-Saccharomyces cerevisiae antibodies.