Alterations of the Human Gut Microbiome in Patients With Hidradenitis Suppurativa: A Case-control Study and Review of the Literature

• Published in: Dermatology practical & conceptual Vol. 12; no. 4; p. e2022191
• Main Authors: Öğüt, Neslihan Demirel, Hasçelik, Gülşen, Atakan, Nilgün
• Format: Journal Article
• Language: English
• Published: Austria Mattioli1885 01-10-2022
• Subjects: gut microbiome; hidradenitis suppurativa; inflammatory skin disorders; pathogenesis; hidradenitis suppurativa; gut microbiome; inflammatory skin disorders
• ISSN: 2160-9381; 2160-9381
• DOI: 10.5826/dpc.1204a191

Hidradenitis suppurativa (HS) is a chronic and systemic inflammatory disease that extends beyond the skin. The role of gut microbiome (GM) alterations in the pathogenesis of inflammatory and autoimmune disorders is remarkable.
Based on the hypothesis that dysbiosis in the GM may trigger systemic inflammation in the pathogenesis of HS, this study aimed to investigate whether the GM is altered in HS patients compared with healthy subjects.
In the present case-control study, fecal samples from 15 patients with HS and 15 age- and sex-matched healthy individuals were collected and analyzed using 16S rRNA-based metagenomic analysis, New Generation Sequencing (NGS). The V3 and V4-hypervariable regions of the bacterial 16S rDNA gene were amplified from all samples and sequenced by the Illumina MiSeq platform. Bioinformatics analyses were performed in QIIME2.
Shannon alpha diversity index showed significantly reduced diversity in HS patients (P = 0.048). Bray-Curtis Dissimilarity and Jaccard Distance revealed that the gut microbial composition of HS patients was significantly distinctive from that of controls (P = 0.01 and P = 0.007, respectively). The relative abundance of unclassified Clostridiales, unclassified Firmicutes, and Fusicatenibacter in HS was significantly lower than that in controls (P = 0.005, P = 0.029, and P = 0.046, respectively).
This study indicated that significant alterations in the GM of HS patients could play a critical role in the pathogenesis of HS and might be a trigger for systemic inflammation. Increased understanding of the pathogenesis of HS will shed light on the new potential therapeutic targets and novel treatment options.