Authors :
Shravan Subhash; Prasanth Hanumanthu; Moin Akhtar Shaik; Deexitha Mudigonda; Umar Saleem
Volume/Issue :
Volume 10 - 2025, Issue 7 - July
Google Scholar :
https://tinyurl.com/23kpypc7
Scribd :
https://tinyurl.com/ukkvcre2
DOI :
https://doi.org/10.38124/ijisrt/25jul896
Note : A published paper may take 4-5 working days from the publication date to appear in PlumX Metrics, Semantic Scholar, and ResearchGate.
Note : Google Scholar may take 30 to 40 days to display the article.
Abstract :
The gut-skin axis has become an important conceptual framework to identify a relationship between gut microbiota
and skin immunity, particularly in autoimmune dermatologic diseases. This narrative review aims to summarize recent data
examining how gut dysbiosis, characterized by low microbial diversity and disruption of each of the gut's microbial communities,
plays a role in the pathogenesis and pathophysiology of psoriasis, systemic lupus erythematosus (SLE), alopecia areata, and
scleroderma. We consider different pathways, including but not limited to increased intestinal permeability ("leaky gut"),
Th17/Treg balance, the presence of and/or development of pro-inflammatory cytokines, and molecular mimicry, for how gut
dysbiosis drives immune dysregulation in the skin. Clinical and translational evidence of microbiome-based therapies with
probiotics, prebiotics, and fecal microbiota transplantation (FMT) has been shown not only to improve disease severity but also
reduce systemic inflammation and restore gut microbiome diversity and community structure. Specific AMR therapies have
indicated differences in PASI, SLEDAI, and inflammatory markers such as IL-6 and TNF-α. This narrative review strongly
affirms that ambient need for more precision-based solutions to prevent and treat autoimmunity using a combination of multi-
omics, gut microbiome profiling, as well as artificial intelligence (AI)-driven individualized solutions. Ultimately, the gut–skin
axis depicts autoimmune skin diseases from single dermatologic disease classifications to systemic immune diseases grounded in
gut health, offering new possibilities for diagnosis, intervention, and disease modulation.
Keywords :
Gut Microbiota; Gut Skin Axis, Immune Modulation; Intestinal Barrier Dysfunction; Psoriasis; SLE; Alopecia Areata; Scleroderma.
References :
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The gut-skin axis has become an important conceptual framework to identify a relationship between gut microbiota
and skin immunity, particularly in autoimmune dermatologic diseases. This narrative review aims to summarize recent data
examining how gut dysbiosis, characterized by low microbial diversity and disruption of each of the gut's microbial communities,
plays a role in the pathogenesis and pathophysiology of psoriasis, systemic lupus erythematosus (SLE), alopecia areata, and
scleroderma. We consider different pathways, including but not limited to increased intestinal permeability ("leaky gut"),
Th17/Treg balance, the presence of and/or development of pro-inflammatory cytokines, and molecular mimicry, for how gut
dysbiosis drives immune dysregulation in the skin. Clinical and translational evidence of microbiome-based therapies with
probiotics, prebiotics, and fecal microbiota transplantation (FMT) has been shown not only to improve disease severity but also
reduce systemic inflammation and restore gut microbiome diversity and community structure. Specific AMR therapies have
indicated differences in PASI, SLEDAI, and inflammatory markers such as IL-6 and TNF-α. This narrative review strongly
affirms that ambient need for more precision-based solutions to prevent and treat autoimmunity using a combination of multi-
omics, gut microbiome profiling, as well as artificial intelligence (AI)-driven individualized solutions. Ultimately, the gut–skin
axis depicts autoimmune skin diseases from single dermatologic disease classifications to systemic immune diseases grounded in
gut health, offering new possibilities for diagnosis, intervention, and disease modulation.
Keywords :
Gut Microbiota; Gut Skin Axis, Immune Modulation; Intestinal Barrier Dysfunction; Psoriasis; SLE; Alopecia Areata; Scleroderma.