Gut-skin dysbiosis as a contributory factor in the comorbidity of atopic dermatitis and hidradenitis suppurativa: A systematic review of shared pathways

Summary: Abstract Body: Atopic dermatitis (AD) and hidradenitis suppurativa (HS) are chronic inflammatory skin conditions. Recent evidence suggests that gut-skin microbiome dysbiosis may contribute to their development and comorbidity.1,2 This review examines the role of gut-skin dysbiosis in AD and HS pathogenesis, focusing on immune dysregulation, barrier impairment, metabolic alterations, and systemic inflammation. A literature search on gut microbiome alterations in AD, HS, or their comorbidity was conducted with a focus on microbial composition, inflammatory markers, and proposed mechanisms. Several shared pathways linking gut dysbiosis to AD and HS comorbidity were identified. In both conditions, immune dysregulation with elevated levels of pro-inflammatory cytokines and altered T-cell responses was reported.3,4 Impaired barrier function due to increased intestinal permeability was found to exacerbate skin inflammation and immune response.5 Reduced short-chain fatty acid production was also associated with systemic inflammatory response.6 Inflammatory pathways, including enhanced NF-κB signaling and increased TNF-α expression, were influenced by gut dysbiosis.7 Microbial shifts were noted, including decreased levels of beneficial Lactobacillus species and increased levels of potentially harmful bacteria.3,6 Studies have shown that patients with HS have a higher risk of developing inflammatory skin conditions, including AD.4 Immunomodulatory analysis revealed that HS exhibits increased expression of TH1,2,17 signatures with no prevalent TH signatures, unlike psoriasis (TH1 and17) and AD (TH2).4 Gut-skin dysbiosis may play a key role in the comorbidity of AD and HS through multiple shared pathways, offering insights into potential therapeutic targets, like prebiotics, probiotics, and microbiome-based therapies.5,7,8 Bryce DeLong¹, Sahil Kapur¹, Kermanjot S. Sidhu², Craig Burkhart¹ 1. The University of Toledo, Toledo, OH, United States. 2. Michigan State University, East Lansing, MI, United States. Innate Immunity, Microbiology, and Microbiome