Microbiota and mycobiota in chronic inflammatory demyelinating polyneuropathy: clinical and pathophysiological correlations

Introduction Chronic inflammatory demyelinating polyneuropathy (CIDP) is an immune mediated neuropathy with incompletely defined triggers and no validated biomarkers. We investigated associations between bacterial and fungal communities, short chain fatty acids (SCFAs), and IL18 promoter variation with clinically/electrophysiologically relevant measures. Methods We enrolled 32 treatment naive CIDP patients and 15 healthy controls. Stool, serum and cerebrospinal fluid (CSF) samples were collected. Disability was assessed using the clinical scale and related to nerve conduction study (NCS) parameters. IL18 promoter variants (rs187238, rs1946518, and rs1946519) were genotyped in haplotype based comparisons. SCFAs were quantified in stool, serum, and CSF. Faecal and CSF microbiota and mycobiota were profiled by amplicon sequencing of the 16S rRNA V3 V4 region and the ITS1 region, respectively. Bioinformatic processing and diversity analyses were performed in QIIME2. Alpha diversity and beta diversity metrics were computed across taxonomic levels. Differential abundance testing was conducted with ANCOM BC2. Results CIDP was characterised by increased faecal bacterial alpha diversity and significant shifts in beta diversity relative to controls. Diversity patterns differed across clinical subgroups, including diabetes status and disability severity. Higher faecal bacterial diversity metrics correlated with greater NCS abnormalities, whereas associations with beta diversity measures were weaker. Taxonomic analyses identified enrichment of Hominisplanchenecus_A faecis and depletion of Lawsonibacter sp000177015 in CIDP. SCFAs concentrations correlated with bacterial diversity indices, and IL18 haplotypes were associated with distinct microbial signatures. Faecal mycobiota showed no robust case control differences in overall diversity. CSF sequencing revealed a low biomass bacterial signal and diversity metrics correlated with neurophysiological measures. Discussion We confirmed the increased gut microbiome alpha diversity in CIDP patients, as observed in previous research. Our findings suggest significant alterations in both gut microbiota and mycobiota during the course of CIDP, which correlate with clinical, electrophysiological, and laboratory parameters.