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HOME > J. Microbiol > Volume 64(1); 2026 > Article
Review
 Obesity, skin disorders, and the microbiota: Unraveling a complex web
Yu Ri Woo, Hei Sung Kim*
Journal of Microbiology 2026;64(1):e2508007.
DOI: https://doi.org/10.71150/jm.2508007
Published online: January 31, 2026

Department of Dermatology, Incheon St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul 06649, Republic of Korea

*Correspondence Hei Sung Kim hazelkimhoho@gmail.com
• Received: August 19, 2025   • Revised: December 4, 2025   • Accepted: December 5, 2025

© The Microbiological Society of Korea

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Obesity is increasingly recognized as a systemic pro-inflammatory condition that influences not only metabolic and cardiovascular health but also the development and exacerbation of cutaneous inflammatory diseases. This review examines the interplay between obesity, microbial dysbiosis, and two archetypal inflammatory skin disorders—hidradenitis suppurativa (HS) and psoriasis. We highlight how obesity-induced changes in immune signaling, gut permeability, and microbiota composition—both in the gut and the skin—contribute to cutaneous inflammation. Special emphasis is placed on shared pathways such as the Th17/IL-23 and IL-22 signaling axes, adipokine imbalance, and microbial metabolites like short-chain fatty acids and lipopolysaccharides. The review critically evaluates the current literature, distinguishing preclinical insights from clinical evidence, and underscores the potential of microbiota-targeted therapies and metabolic interventions as adjunctive treatment strategies. By integrating metabolic, immunologic, and microbiome data, we synthesize emerging evidence to better understand the gut–skin–obesity interplay and guide future therapeutic innovations.
  • Keywords: obesity, hidradenitis suppurativa, psoriasis, gut–skin axis, microbiota, dysbiosis, Th17, IL-22
Obesity, both a chronic inflammatory condition and metabolic disorder, has become a major global health concern with rising prevalence. Obesity is defined by the World Health Organization as a body mass index (BMI) of 30 kg/m2 or more, and is linked to increased risks of cardiovascular disease, insulin resistance, and systemic inflammation. Beyond these metabolic outcomes, obesity exerts profound effects on the skin—both structurally and immunologically—manifesting in increased severity and prevalence of various dermatologic conditions. Among these, hidradenitis suppurativa (HS) and psoriasis stand out as chronic inflammatory dermatoses most consistently linked to obesity, both epidemiologically and mechanistically (Hirt et al., 2019).
Recent advances have highlighted the role of the human microbiota—particularly that of the gut and skin—as a key mediator in the bidirectional relationship between obesity and these inflammatory skin diseases. Microbial dysbiosis may serve as both a marker and a modulator of disease activity, with alterations in microbial metabolites, such as short-chain fatty acids (SCFAs) and lipopolysaccharide (LPS), contributing to systemic inflammation and immune dysregulation (Asadi et al., 2022). Simultaneously, the gut-skin axis has emerged as a compelling model to explain how microbial and metabolic disturbances in obesity can impact cutaneous immunity (Aron-Wisnewsky et al., 2021).
Among the most critical immunologic links is the activation of the Th17/interleukin (IL)-23 and IL-22 pathways, which promote keratinocyte proliferation, barrier disruption, and inflammatory cytokine release (Hirt et al., 2019). These axes serve as common mechanistic threads in the pathogenesis of HS and psoriasis, both of which are characterized by neutrophilic inflammation and perturbed barrier function.
While prior integrative reviews have primarily emphasized on skin physiology (Darlenski et al., 2022; Yosipovitch et al., 2007), this article differs by systematically synthesizing recent skin and gut microbiome evidence, including metagenomic and functional studies, contrasting obesity-driven versus disease-specific microbial changes, and discussing therapeutic strategies that target the microbiota–metabolism–skin axis. In doing so, this review positions the microbiome as a key link in the gut-skin-obesity triad and evaluates its translational potential for novel interventions.
In individuals with obesity, the skin undergoes a variety of functional and structural changes resulting from both local and systemic effects of excessive adiposity. These changes are not superficial manifestations but reflect the pathophysiological consequences of metabolic inflammation, immune dysregulation, and microbiota alterations. Understanding these changes is essential for clarifying how obesity contributes to skin disease onset, severity, and chronicity.
Impaired skin barrier function
Obesity-related shifts in epidermal physiology affect skin barrier integrity and hydration, though study findings remain mixed. Transepidermal water loss (TEWL) has been positively associated with BMI in recent studies, and Mendelian randomization data suggest a causal link (Yew et al., 2023). This impairment may be linked to obesity-induced low-grade inflammation, altered lipid synthesis, and cytokine-driven disruption of tight junction proteins—especially via IL-6, tumor necrosis factor (TNF)-α, and IL-22, which are overexpressed in obesity and known to affect keratinocyte differentiation (Hirt et al., 2019).
Sebaceous and apocrine/eccrine gland activity
Obesity alters sebaceous, eccrine, and apocrine gland function through hormonal and adipokine imbalances. Elevated insulin-like growth factors and androgens stimulate sebaceous proliferation and sebum production, while increased leptin and reduced adiponectin promote sebocyte inflammation (Abulnaja, 2009; Deplewski and Rosenfield, 1999; Izquierdo et al., 2019; Jung et al., 2017). Eccrine activity is heightened, causing excessive sweating in skin folds and favouring microbial shifts (Adams et al., 2015). Apocrine secretions, metabolized by skin microbiota, contribute to body odour, with axillary osmidrosis more common in individuals with high BMI (Dong et al., 2021).
Wound healing and collagen remodeling
Obesity is associated with impaired wound healing and altered collagen architecture. Insufficient collagen synthesis relative to skin expansion leads to reduced tensile strength and disorganized fibers, as shown in both human and animal studies (do Nascimento and Monte-Alto-Costa, 2011; Enser and Avery, 1984; Matsumoto et al., 2014). Chronic low-grade inflammation in adipose tissue alters fibroblast activity and increases the expression of matrix metalloproteinases, contributing to defective collagen deposition and tissue remodeling (Pierpont et al., 2014). Concurrently, vascular insufficiency and localized hypoxia further delay re-epithelialization and collagen maturation, while skin microbial dysbiosis and reduced innate immunity heighten infection risk (Larouche et al., 2018; Pierpont et al., 2014). Collectively, these factors create an adverse dermal microenvironment that hinders effective tissue repair.
Vascular and lymphatic alterations
Obesity impairs cutaneous vascular and lymphatic function. Microvascular reactivity is reduced, driven by elevated free fatty acids (FFAs), TNF-α, and decreased adiponectin, which compromise endothelial integrity (de Jongh et al., 2004; Kern et al., 2003). Venous hypertension from intra-abdominal pressure and valve incompetence increases vascular stress, contributing to stasis dermatitis, varicose veins, and atrophie blanche (Danielsson et al., 2002; Sugerman, 2001). Excess adiposity also disrupts lymphatic drainage, causing edema, hypoxia, and cytokine accumulation (Kataru et al., 2020). Mechanistically, obesity reduces lymphatic vessel contractility, increases endothelial permeability, and alters lymphatic endothelial cell (LEC) gene expression, thereby sustaining inflammation and tissue remodeling, which may aggravate conditions such as HS and chronic venous insufficiency (Kataru et al., 2020).
Skin microbiota in obesity
Healthy human skin harbors a diverse array of microbial communities, with composition varying by anatomical site, sebaceous activity, and environmental exposure. Dominant bacterial genera in healthy skin includes Cutibacterium, Staphylococcus, Corynebacterium, and fungi such as Malassezia. In healthy skin, the volar forearm skin microbiome is predominantly composed of Cutibacterium acnes, Staphylococcus epidermidis, and various Streptococcus species (Shi et al., 2016), and post-pubertal increases in sebum production selectively support colonization by lipophilic microbes like Cutibacterium and Corynebacterium.
Despite the known impact of obesity on gut microbiota, relatively few studies have explored its effect on skin microbiome in obesity (Brandwein et al., 2019; Ma et al., 2024; Rood et al., 2018; Vongsa et al., 2019; Walker et al., 2020). In a 2019 exploratory study, 40 female participants were stratified by BMI to compare microbial composition in exposed (abdominal) versus unexposed (vulvar) skin (Vongsa et al., 2019). High BMI was associated with elevated pH and increased colonization by Finegoldia and Corynebacterium in the vulvar region, while abdominal skin showed minimal BMI-related differences (Vongsa et al., 2019). This suggests that obesity may more profoundly affect microbiota in occluded or moist anatomical regions.
Larger cohort studies further support obesity-associated shifts in cutaneous microbial composition. An analysis of 822 skin samples from the American Gut Project found that individuals with lower BMI harbored greater microbial diversity across various skin sites, with underweight individuals showing broader microbial richness than those with obesity (Brandwein et al., 2019). The study also reported a positive correlation between BMI and the abundance of Corynebacterium, reinforcing the potential role of adiposity in promoting the colonization of specific microbial taxa (Brandwein et al., 2019). A recent cohort study in China, examined the facial skin microbiome and physiological parameters in 198 healthy women aged 18 to 35 years (Ma et al., 2024). This study found that higher BMI was associated with impaired skin barrier function, indicated by increased TEWL and decreased skin surface pH (Ma et al., 2024). Notably, facial skin bacterial and fungal diversity was increased in the overweight group, with higher abundances of Streptococcus, Corynebacterium, Malassezia, and Candida compared to individuals with normal BMI (Ma et al., 2024). There were also significant negative correlations between skin pH and relative abundances of Malassezia and Candida, suggesting complex interactions between skin physiology and microbial communities (Ma et al., 2024). Unlike Brandwein et al. (2019)’s study, which surveyed multiple skin sites mainly in a U.S. population, the Shanghai study focused on facial skin in an East Asian cohort. The findings underscore how anatomical site, ethnicity, and geographic context can shape obesity-associated changes in the skin microbiota.
Together, these findings indicate that obesity alters cutaneous microbial communities by modifying the chemical and physical microenvironment of the skin. Changes in skin surface pH, hydration, sweat composition, and occlusion may collectively shape microbial diversity and promote the overgrowth of Corynebacterium and other opportunistic taxa. These obesity-related microbial and physiological shifts may predispose the skin to inflammation, barrier disruption, and dysbiosis, potentially amplifying the severity of obesity-associated dermatoses (Table 1).
Obesity is increasingly recognized as a systemic inflammatory and metabolic condition that extends its influence far beyond traditional cardiometabolic comorbidities. Accumulating evidence demonstrates that excess adiposity has profound effects on cutaneous immunity and disease expression, contributing to both the onset and exacerbation of chronic inflammatory skin disorders (Fig. 1). Among these, HS and psoriasis are the conditions most consistently linked to obesity, with both epidemiologic and mechanistic studies supporting a strong bidirectional relationship.
Epidemiologic data consistently demonstrate higher prevalence and increased severity of both HS and psoriasis in individuals with obesity (Carrascosa et al., 2014; Kromann et al., 2014). Obesity also reduces responsiveness to biologics and conventional systemic therapies, likely due to altered pharmacokinetics, intensified baseline inflammation, and persistent metabolic dysfunction. This bidirectional interplay between skin disease and obesity—where chronic inflammation contributes to sedentary behavior, weight gain, and worsening metabolic health, creates a reinforcing cycle that complicates long-term management.
Although HS and psoriasis present distinct clinical phenotypes—one characterized by follicular occlusion followed by rupture and secondary immune activation (Krajewski et al., 2023), the other by epidermal hyperproliferation and plaque formation (Carrascosa et al., 2014)—both diseases are strongly shaped by obesity-related immunometabolic disturbances. Excess adipose tissue actively produces proinflammatory cytokines (e.g., TNF-α, IL-6, IL-1β) and chemokines. At the same time, obesity induces characteristic alterations in adipokine secretion—characterized by elevated leptin and resistin and reduced adiponectin—promotes Th1/Th17 polarization, NF-κB activation, and metabolic inflammation that drives insulin resistance (González-López et al., 2020; Kyriakou et al., 2018). These systemic alterations converge on inflammatory pathways implicated in HS and psoriasis, particularly the Th17/IL-23 axis, which drives keratinocyte proliferation, neutrophil recruitment, and barrier disruption (Fletcher et al., 2020; van Straalen et al., 2022).
Leptin promotes Th1/Th17 differentiation and correlates with disease severity; resistin amplifies NF-κB–mediated inflammation; and reduced adiponectin decreases IL-10 and weakens counter-regulation of TNF-α and IL-6 (González-López et al., 2020; Kyriakou et al., 2018; Malara et al., 2018; Seth et al., 2020). These obesity-associated adipokine shifts reinforce systemic inflammation that, in turn, amplifies cutaneous immune activation. Elevated levels of IL-1β, IL-6, IL-17, and TNF-α contribute to follicular rupture and sinus tract formation in HS (Krajewski et al., 2023), and drive keratinocyte proliferation and plaque development in psoriasis (Carrascosa et al., 2014).
Obesity also alters fundamental aspects of skin physiology, further linking excess weight to disease severity. Mechanical stress in intertriginous regions, exacerbated by central adiposity, follicular occlusion, and microinjury in HS (Mintoff et al., 2023), while impaired barrier function and altered hydration states associated with obesity can intensify psoriatic inflammation.
Microbiome-level changes further reinforce these mechanisms. Obesity-associated gut dysbiosis, characterized by increased intestinal permeability and metabolic endotoxemia, leads to enhanced LPS–TLR4 signaling and Th17-skewed immunity (Cani et al., 2007; Wang et al., 2012). Concurrently, skin microbiome alterations—including increased Corynebacterium, Finegoldia, and Staphylococcus in occluded sites—mirror patterns observed in HS and psoriasis (Chang et al., 2018; Vongsa et al., 2019), suggesting shared microbial pathways linking systemic metabolism to local cutaneous inflammation.
Obesity-driven immunometabolic disturbances shape the inflammatory milieu of both HS and psoriasis, but these effects are further compounded by disease-specific and shared alterations in the cutaneous microbiome. Because the skin’s microbial communities interact intimately with the barrier, sebaceous and sweat gland function, and local immune signaling—all of which are profoundly modulated by obesity—microbiome dysregulation has emerged as a critical mechanistic bridge linking systemic metabolic dysfunction with cutaneous inflammation. The following section reviews how obesity intersects with disease-specific patterns of skin microbiota dysbiosis in HS and psoriasis and how these microbial changes may contribute to disease chronicity and severity.
Obesity-driven immunometabolic disturbances shape the inflammatory milieu of both HS and psoriasis, but these effects are further compounded by disease-specific and shared alterations in the cutaneous microbiome. Because the skin’s microbial communities interact intimately with the barrier, sebaceous and sweat gland function, and local immune signaling—all of which are profoundly modulated by obesity—microbiome dysregulation has emerged as a critical mechanistic bridge linking systemic metabolic dysfunction with cutaneous inflammation. The following section reviews how obesity intersects with disease-specific patterns of skin microbiota dysbiosis in HS and psoriasis and how these microbial changes may contribute to disease chronicity and severity.
Growing evidence indicates that dysbiosis of the skin microbiota is a shared feature of inflammatory skin diseases, including HS and psoriasis. Although these disorders present distinct clinical and immunologic profiles, both exhibits reduced microbial diversity, expansion of opportunistic or inflammation-associated taxa, and depletion of protective commensals (Guet-Revillet et al., 2017; Haskin et al., 2016; Naik et al., 2020). These alterations interact with obesity-related changes in skin physiology—such as increased humidity in skin folds, altered sebum composition, and barrier impairment—to amplify local inflammation and disease chronicity.
Across both HS and psoriasis, multiple studies report an increased abundance of Corynebacterium, Staphylococcus, and various facultative or obligate anaerobes, along with a consistent reduction in Cutibacterium, a dominant commensal associated with lipid homeostasis and barrier integrity (Chang et al., 2018; Schneider et al., 2020). The loss of Cutibacterium may weaken colonization resistance and enhance antigenic exposure to the immune system, contributing to heightened local inflammation.
Obesity appears to accentuate these dysbiotic patterns. Obese HS patients, for example, are significantly more likely to exhibit Firmicutes-dominant skin flora compared with non-obese HS patients (Haskin et al., 2016). Similar BMI-associated increases in Corynebacterium and Staphylococcus have been observed in occluded or high-sebum regions in other cohorts, suggesting shared microenvironmental effects of obesity across inflammatory dermatoses.
HS shows a particularly prominent enrichment of anaerobic, proteolytic, and biofilm-forming bacteria in intertriginous regions (Ring et al., 2019). Studies consistently report increased representation of Porphyromonas, Prevotella, Peptoniphilus, Anaerococcus, Finegoldia magna, and Fusobacterium in HS lesions (Guet-Revillet et al., 2017; McCarthy et al., 2022; Ring et al., 2017). Importantly, taxa such as Fusobacterium and Parvimonas correlate with greater disease severity, especially in Hurley stage III disease. Notably, lesional and non-lesional HS skin often share similar dysbiotic profiles (Schneider et al., 2020), reflecting a “field effect” driven by chronic inflammation, occlusion, and persistent microenvironmental dysfunction. This pattern is characterized by enrichment of opportunistic anaerobes—such as Porphyromonas, Anaerococcus, and Peptoniphilus—together with a marked depletion of Cutibacterium (Schneider et al., 2020).
In psoriasis, dysbiosis is typically characterized by altered proportions of aerobic or aerotolerant genera. Lesional plaques often display increased levels of Streptococcus, Staphylococcus, and Corynebacterium alongside reduced Cutibacterium (Chang et al., 2018). Emerging multi-omics data highlight Corynebacterium simulans as a taxon linked to antiviral/interferon pathways and greater disease severity. Therapeutic modulation of the microbiome has also been observed: IL-17A inhibitor treatment partially restores functional microbial pathways, with improvements in methionine and tryptophan metabolism aligning toward healthy skin profiles (Lv et al., 2025).
Collectively, these findings show that while HS demonstrates an anaerobe-dominant, biofilm-rich dysbiosis, and psoriasis a Streptococcus/Staphylococcus/Corynebacterium-enriched profile, both share key unifying features (Fig. 2). These overlapping microbial perturbations likely contribute to impaired barrier function, enhanced antigen presentation, and persistent immune activation, helping to explain the chronic, relapsing nature of both HS and psoriasis—particularly in individuals with obesity.
Obesity-associated gut dysbiosis is not defined by a uniform phylum-level signature—Firmicutes/Bacteroidetes shifts are heterogeneous across cohorts and methods—whereas small but recurrent reductions in α-diversity and, more robustly, functional perturbations (e.g., impaired SCFA production, lower butyrate-producing capacity, increased endotoxaemia, bile-acid/indole pathway changes) are observed more consistently (Cheng et al., 2022; Coppola et al., 2021; Duncan et al., 2008; Koliada et al., 2017; Ley et al., 2006; Sze and Schloss, 2016). Causality is supported by gnotobiotic transfers: obese-donor communities increase adiposity in germ-free mice and transmit an “obese” phenotype in twin-discordant models unless outcompeted by lean taxa (Ridaura et al., 2013; Turnbaugh et al., 2006).
High-fat feeding increases gut permeability and lipopolysaccharide (LPS), driving “metabolic endotoxaemia”; blocking LPS–CD14/TLR4 protects against weight gain/insulin resistance (Cani et al., 2007). High-dose LPS can drive Th17 differentiation through dendritic-cell–dependent signaling, suggesting that LPS elevations in obesity may similarly enhance Th17-mediated systemic and cutaneous inflammation (Wang et al., 2012).
In addition, butyrate induces colonic FOXP3⁺ Tregs/IL-10 via histone deacetylase (HDAC) inhibition, while propionate/succinate trigger intestinal gluconeogenesis and a portal–vagal circuit improving glycaemia and energy balance—pathways that can temper Th17/IL-23 tone (De Vadder et al., 2014; Furusawa et al., 2013; Yoshida et al., 2019).
Gut microbes transform bile acids, which can signal through FXR and TGR5 pathways. This stimulates intestinal L-cells to release glucagon-like peptide (GLP)-1, enhancing satiety and glucose control and thereby supporting resistance to obesity. Antibiotic disruption of the microbiota abolishes these benefits (Pathak et al., 2018). Bariatric surgery remodels BA–microbiota networks, and post-operative communities transfer leanness to mice (Liou et al., 2013).
Bacterial indoles activate aryh hydrocarbon receptor (AhR), boosting IL-22 and intestinal barrier repair, a mechanism that may protect against obesity-associated low-grade inflammation (Zelante et al., 2013). In contrast, gut dysbiosis in obesity can enrich pathways for branched-chain amino acid (BCAA) biosynthesis (notably linked to Prevotella copri) and increase levels of imidazole propionate, a microbial metabolite that impairs insulin signalling and reduces responsiveness to metformin, thereby exacerbating obesity-related insulin resistance and metabolic dysfunction (Koh et al., 2018; Natividad et al., 2018; Pedersen et al., 2016; Zelante et al., 2013).
Growing evidence suggests that gut microbial dysbiosis contributes to the systemic immune activation observed in both psoriasis and HS. Although findings vary across studies due to differences in geography, sequencing approaches, and the strong confounding impact of obesity, several reproducible taxonomic and functional signatures have emerged across these conditions. Overall, psoriasis and HS both displays altered microbial composition, disrupted metabolic pathways, and enrichment of proinflammatory microbial metabolites, supporting the existence of an intestinal inflammatory axis that may influence cutaneous disease expression.
Many cohorts demonstrate an increased Firmicutes-to-Bacteroidetes ratio (Chen et al., 2018; Dei-Cas et al., 2020; Shapiro et al., 2019), although some studies report the opposite shift (Huang et al., 2019; Wen et al., 2023), underscoring the influence of population- and diet-related variability. Functional analyses consistently indicate over-representation of pathways related to chemotaxis and carbohydrate transport (Chen et al., 2018), lipopolysaccharide biosynthesis, WNT signaling, apoptosis, bacterial secretion systems, and phosphotransferase systems (Chen et al., 2018; Xiao et al., 2021). Psoriatic fecal metabolomic profiles frequently show elevated levels of hydrogen sulfide, isovalerate, isobutyrate, hyaluronan, and hemicellulose (Xiao et al., 2021), suggesting heightened microbial metabolic activity that may promote epithelial dysfunction and amplify immune activation. Importantly, when analyses are adjusted for BMI, microbial alterations become more distinct, indicating that obesity may obscure psoriasis-specific dysbiosis (Chen et al., 2018). Therefore, longitudinal and multi-omics studies in lean psoriasis cohorts will be essential to disentangle adiposity-related effects from disease-specific microbial signatures.
HS also exhibits significant gut microbial dysregulation, although the pattern differs somewhat from psoriasis. Several studies describe reduced alpha diversity in HS (Kam et al., 2021; Öğüt et al., 2022), while others report comparable diversity but distinct compositional shifts (Lelonek et al., 2025). Specifically, HS was linked to reduced abundance of several commensal taxa (e.g., Collinsella, Clostridia, Lachnospiraceae) and enrichment of potentially pathogenic or opportunistic genera (e.g., Enterorhabdus, Holdemanella, Comamonas, Enterobacter) (Lelonek et al., 2025). Disease severity further influenced microbial composition, with higher odds of occurrence reported for certain genera such as Chloroplast, Dielma, Eisenbergiella, and Paludicola (Lelonek et al., 2025). Approximately 40% of HS patients possess a “Crohn-like” gut microbial signature—a configuration marked by enrichment of pathogenic genera such as Enterococcus, Veillonella, Escherichia/Shigella, and a pronounced loss of beneficial taxa like Faecalibacterium (Cronin et al., 2023). This microbial pattern is associated with decreased levels of the anti-inflammatory mediator growth-arrest specific 6 (GAS6) and elevated systemic inflammatory cytokines, particularly interleukin-12 (IL-12) (Cronin et al., 2023), suggesting potential overlap between HS and gastrointestinal inflammatory disorders.
Additional findings further support the concept of microbiome-driven immune dysregulation in HS. The absence of Bifidobacterium adolescentis (B. adolescentis) in adults but its presence inf all pediatric HS patients, suggests disrupted age-related maturation of the gut microbiome (Collard et al., 2025). In addition, causal inference analysis suggested that specific gut taxa may differentially influence HS risk: the Clostridium innocuum group and Lachnospira were associated with potential risk-promoting (anti-protective) effects, whereas Family XI and Porphyromonadaceae appeared to confer protective influences (Liu et al., 2024). Collectively, these observations suggest that HS-associated gut dysbiosis is defined less by uniform reductions in diversity and more by distinct taxonomic and functional disruptions that track with disease severity and systemic inflammation.
Taken together, the gut microbiome in psoriasis and HS displays both shared and disease-specific abnormalities. Both conditions exhibit functional dysbiosis characterized by increased LPS-related pathways, altered SCFA-related metabolism, enrichment of inflammatory microbial metabolites, and depletion of beneficial commensals (Cani et al., 2007; Cronin et al., 2023; Xiao et al., 2021). Psoriasis is more frequently associated with perturbations in Firmicutes and shifts in carbohydrate- and LPS-related metabolic pathways (Chen et al., 2018; Xiao et al., 2021), while HS shows stronger links to Crohn-like signatures, loss of Faecalibacterium, and enrichment of proinflammatory pathobionts (Cronin et al., 2023; Lelonek et al., 2025). These convergent microbial disturbances may promote systemic inflammation, enhance Th17/IL-23 signaling (Wang et al., 2012), and contribute to the chronic, relapsing nature of both skin diseases—particularly in individuals with obesity, where metabolic endotoxemia and increased intestinal permeability further amplify gut–skin immune cross-talk (Cani et al., 2007).
Lifestyle modifications and weight management
Given the strong correlation between obesity and various dermatologic conditions, weight management forms the cornerstone of therapeutic interventions. Numerous studies suggest that weight reduction can significantly improve disease severity in both HS and psoriasis. A comprehensive review reported that weight loss interventions are associated with symptom improvement in HS, especially in friction-prone areas (Boer, 2016; Sivanand et al., 2020). In psoriasis, a meta-analysis demonstrated that non-pharmacologic weight reduction strategies lead to significant improvement in disease severity among overweight and obese individuals (Upala and Sanguankeo, 2015).
Because dietary composition is one of the strongest determinants of gut microbial structure, dietary modifications such as low glycemic-load diets and adherence to Mediterranean dietary patterns have shown benefit in reducing systemic inflammation and improving skin conditions associated with metabolic syndrome. These lifestyle interventions likely exert their effects not only through metabolic pathways but also through reshaping gut microbial communities.
Microbiota-targeted therapies
With growing recognition of the gut–skin axis, microbiota-targeted interventions—including prebiotics, probiotics, synbiotics, and postbiotics—are gaining attention as potential adjunctive therapies for obesity-associated skin diseases. These interventions aim to restore microbial balance in both the gut and skin, thereby mitigating systemic inflammation and improving cutaneous outcomes.
In psoriasis, a randomized controlled trial showed that a 12-week oral probiotic formulation containing Bifidobacterium longum CECT 7347, B. lactis CECT 8145, and Lactobacillus rhamnosus CECT 861 resulted in up to a 75% reduction in PASI scores (Navarro-López et al., 2019). Although clinical evidence specifically targeting obesity-associated skin diseases is limited, shared features of dysbiosis across obesity, psoriasis, and HS—such as reduced microbial diversity, a lower abundance of Bacteroidetes, and a relative increase in Firmicutes—provide strong biological plausibility.
Microbiota-directed interventions may benefit both obesity and skin inflammation through convergent immunometabolic pathways. Probiotics, prebiotics, and dietary fiber supplementation increase the production of short-chain fatty acids (SCFAs), enhance intestinal barrier integrity, and reduce metabolic endotoxemia (Abulnaja, 2009; Li et al., 2024; Mishra et al., 2023; Zhao et al., 2018), thereby suppressing systemic low-grade inflammation that drives metabolic dysfunction and Th17-skewed skin inflammation. Restoration of microbial diversity also modulates IL-23/IL-17 signaling and improves adipose–immune crosstalk, offering a unified mechanism through which microbial modulation can influence both metabolic and dermatologic outcomes.
Bidirectional interactions between the skin barrier and gut microbiome While it is well established that gut dysbiosis can influence skin inflammation, emerging data suggest that skin barrier disruption can also affect gut microbial ecology. In a landmark study, Dokoshi et al. (2024) demonstrated that mechanical skin injury or epidermal overexpression of hyaluronidase in mice led to significant alterations in the gut microbiota, including reduced diversity, loss of beneficial species, and increased susceptibility to DSS-induced colitis. Mechanistically, skin damage released dermal hyaluronan fragments, which acted as damage-associated molecular patterns (DAMPs), inducing intestinal expression of Reg3 and Muc2, and altering colon microbial composition—even in germ-free mice (Dokoshi et al., 2024). These findings underscore the complex and reciprocal nature of the microbiota–metabolism–skin network, in which interventions targeting one barrier tissue may have therapeutic consequences for another.
Pharmacological interventions
Pharmacologic treatments that target metabolic dysfunction not only improve weight and glycemic control but may also alleviate chronic inflammatory skin conditions via immunometabolic and potentially microbiome-mediated mechanisms. Table 2 highlights key studies evaluating the therapeutic effects of various metabolic-targeting interventions on obesity-associated dermatoses.
A meta-analysis confirmed the efficacy of pioglitazone, an oral antidiabetic agent, in improving psoriasis severity. Patients treated with pioglitazone alone achieved superior Psoriasis Area and Severity Index (PASI) 75 responses compared to placebo (OR 8.74; 95% CI, 3.76–20.31), and those on combination therapy (pioglitazone plus standard psoriasis treatment) also demonstrated enhanced outcomes (OR 4.64; 95% CI, 2.03–10.60) (Chang et al., 2020). Additional studies reported concurrent improvements in both metabolic parameters and psoriasis severity in overweight and obese patients treated with pioglitazone (Ghiasi et al., 2019; Lajevardi et al., 2015; Singh and Bhansali, 2016).
GLP-1 receptor agonists such as semaglutide and liraglutide, approved for obesity and diabetes, have also shown promise in treating skin disorders. A meta-analysis involving 32 psoriasis patients with type 2 diabetes across four trials reported that liraglutide therapy significantly decreased psoriasis severity (Chang et al., 2022).
A broader review of longitudinal cohorts and randomized controlled trials (RCTs) on GLP-1RAs revealed PASI improvement in four out of five studies (Ahern et al., 2013; Buysschaert et al., 2014; Faurschou et al., 2015; Lin et al., 2022; Xu et al., 2019). For instance, a RCT by Faurschou et al. (2015) in glucose-tolerant, overweight psoriasis patients did not show significant improvement in week 8. However, another RCT by Lin et al. (2022) involving 25 diabetic patients with a mean BMI of 24, demonstrated significant improvement in both PASI and Dermatology Life Quality Index (DLQI) at 12 weeks. Case reports on semaglutide also noted marked PASI improvement.
In HS, liraglutide treatment in a small cohort of 14 obese patients unresponsive to standard therapy resulted in clinical improvement, especially in those achieving significant weight loss (Nicolau et al., 2023).
Current evidence linking obesity, microbiome alterations, and inflammatory skin diseases is limited by several factors. Most studies are observational and cross-sectional, making causal inference difficult and leaving findings vulnerable to confounding by diet, medications, lifestyle, and genetic predisposition. Substantial methodological variability across microbiome studies—including differences in sampling sites, sequencing approaches, and analytic pipelines—further reduces reproducibility and complicates comparisons between cohorts. Obesity itself also acts as a major confounder, often obscuring disease-specific microbial signatures in HS and psoriasis. Additionally, geographic, ethnic, and anatomical variability limit generalizability. These constraints highlight the need for longitudinal, BMI-adjusted, and multi-omics studies to clarify mechanistic pathways and strengthen translational relevance.
This review underscores the intricate interplay between obesity, gut and skin microbiota, and inflammatory skin diseases such as HS and psoriasis. Current evidence suggests that obesity is not only a metabolic and immunologic driver of skin inflammation but also a modifier of microbial communities, thereby amplifying disease onset, severity, and chronicity. These findings highlight the gut–skin–obesity interplay as a unifying framework linking systemic metabolic status with local cutaneous immune responses and microbial dysbiosis. These insights position the gut–skin–obesity axis as a unifying framework that links systemic metabolic status with cutaneous immune responses and microbial dysbiosis. Future research integrating longitudinal designs, BMI-adjusted analyses, and multi-omics approaches will be essential for identifying functional microbial pathways and advancing microbiota- and metabolism-targeted therapeutic interventions. Ultimately, a deeper understanding of these interconnected systems may enable more precise and effective strategies for managing obesity-associated inflammatory skin diseases.
Fig. 1.
Schematic illustration depicting the bidirectional interactions between obesity and inflammatory skin diseases, highlighting shared immunologic, metabolic, and microbial pathways.
jm-2508007f1.jpg
Fig. 2.
Alterations in the skin and gut microbiome across obesity, psoriasis, and hidradenitis suppurativa (HS).
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Table 1.
Summary of studies investigating the impact of obesity on skin microbiota
Author Sample size Methods Key findings Limitation
Healthy individuals
 Brandwein et al. (2019) 822 skin samples 16S rRNA V4 sequencing Skin microbiome beta diversity and relative abundance of Corynebacterium positively correlated with BMI. BMI self-reported; cross-sectional design; no control for comorbidities; Specific skin area could not be identified
 Rood et al. (2018) 31 obese and 27 normal-weight pregnant women 16S rRNA V1-V3 sequencing In the mid-abdomen and Pfannenstiel area, obese individuals had higher levels of Firmicutes and Bacteroidetes, and lower levels of Actinobacteria compared to controls. Small sample size; pregnant women only (reduced generalizability); potential confounders (pregnancy-related factors, surgical prep. antibiotics) not fully controlled
 Vongsa et al. (2019) 20 women with high BMI (≥ 30), 20 with normal BMI 16S rRNA V1-V3 sequencing Women with normal BMI showed Lactobacillus-dominant flora; those with high BMI had more Finegoldia and Corynebacterium, particularly in the vulvar region. No significant differences were noted in abdominal skin. Limited to female subjects; region-specific sampling (vulvar/abdominal), potential confounders (ethnicity, diet, hygiene practices, and hormonal variation) were not fully adjusted.
 Walker et al. (2020) 10 obese (BMI 35–50) postmenopausal women, 10 normal-weight (BMI 18.5–26.9) women 16S rRNA V1-V3 sequencing Minimal differences in overall skin microbiome composition between groups (mid lower abdomen). Very small cohort; postmenopausal women only (reduced generalizability); potential confounders (ethnicity, diet, hygiene products, sexual activity, antibiotic history and hormonal variation) not fully adjusted.
 Ma et al. (2024) 198 healthy Chinese women 16S rRNA V3-V4 sequencing Higher BMI associated with impaired skin barrier (increased TEWL, decreased pH), increased bacterial and fungal diversity. Overweight group had elevated Streptococcus, Corynebacterium, Malassezia, Candida abundance. Significant correlations observed between skin physiology and microbial composition. Single anatomical site (face); cross-sectional design
HS
 Haskin et al. (2016) 632 HS patients Bacterial culture of purulent drainage The odds of detecting Firmicutes were 3.1 times higher in obese HS patients than in non-obese counterparts. Culture-based (bias against unculturable bacteria); lack of control; potential confounders (antibiotic exposure and comorbidities) are not systematically controlled.

Abbreviation: BMI, body mass index; HS, hidradenitis suppurativa; RNA, Ribonucleic acid.

Table 2.
Summary of longitudinal cohort studies and randomized controlled trials (RCTs) evaluating the effects of obesity-targeted pharmacologic interventions on psoriasis and hidradenitis suppurativa (HS)
Author Study design Sample size Intervention Key findings Limitation
Psoriasis: Liraglutide
 Buysschaert et al. (2014) Prospective cohort 7 patients with type 2 DM and psoriasis 18 weeks of exenatide (5 μg BID) or liraglutide (1.2 mg daily) Mean PASI decreased from 12.0 to 9.2 Very small, uncontrolled case-series; Treatment & co-therapy heterogeneity; short follow-up
 Ahern et al. (2013) Prospective cohort 7 patients with type 2 DM and psoriasis 10 weeks of liraglutide (1.2 mg daily) Median PASI decreased from 4.8 to 3.0; DLQI from 6.0 to 2.0 Small open-label study without controls; low baseline disease activity; confounding by metabolic changes and co-therapies
Faurschou et al. (2015) RCT 20 psoriasis patients 8 weeks of liraglutide (1.2 mg daily) vs. placebo No significant difference in PASI and DLQI between groups Small sample size and short treatment duration; no significant PASI/DLQI benefit over placebo
 Xu et al. (2019) Prospective cohort 7 patients with type 2 DM and psoriasis 12 weeks of liraglutide (1.2 mg daily) Mean PASI dropped from 15.7 to 2.2; DLQI from 21.6 to 4.1 Very small, uncontrolled study; short follow-up; potential confounders for metabolic and treatment regimens for diabetes
 Lin et al. (2022) RCT 25 psoriasis patients with type 2 DM 12 weeks of liraglutide vs. placebo Significant PASI improvement in treatment vs. control group Small, single-center, open-label trial; short follow-up; confounding by metabolic effects
Psoriasis: Pioglitazone
 Singh and Bhansali et al. (2016) RCT 60 psoriasis patients with MS 12 weeks of pioglitazone vs. metformin vs. placebo Significant improvement in PASI, PGA, and ESI with pioglitazone and metformin Single center, open label study; short treatment window
 Ghiasi et al. (2019) RCT 60 psoriasis patients with MS 10 weeks of phototherapy + pioglitazone vs. phototherapy + placebo Greater PASI reduction in pioglitazone group Single center study; short treatment window; fixed-dose design
 Lajevardi et al. (2015) RCT 44 psoriasis patients 16 weeks of MTX + pioglitazone vs. MTX alone PASI75 achieved in 63.6% (combo) vs. 9.1% (MTX alone) Assessor-blinded only; single center trial with small sample size; male-predominant cohort
HS: Liraglutide
 Nicolau et al. (2023) Prospective cohort 14 HS patients with obesity 12 weeks of liraglutide (3 mg) Significant reductions in BMI, Hurley stage, and DLQI Small sample size; short follow-up duration; lack of a control or placebo group

Abbreviation: DLQI, dermatology life quality index; DM, diabetes mellitus; ESI, erythema, scaling, and induration; MS, metabolic syndrome; MTX, methotrexate; PASI, psoriasis area and severity index; PGA, physician global assessment; RCT, randomized placebo-controlled trial.

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        Obesity, skin disorders, and the microbiota: Unraveling a complex web
        J. Microbiol. 2026;64(1):e2508007  Published online January 31, 2026
        DOI: https://doi.org/10.71150/jm.2508007
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      Figure
      Obesity, skin disorders, and the microbiota: Unraveling a complex web
      Image Image
      Fig. 1. Schematic illustration depicting the bidirectional interactions between obesity and inflammatory skin diseases, highlighting shared immunologic, metabolic, and microbial pathways.
      Fig. 2. Alterations in the skin and gut microbiome across obesity, psoriasis, and hidradenitis suppurativa (HS).

      Fig. 1.

      Fig. 2.

      Obesity, skin disorders, and the microbiota: Unraveling a complex web
      Author Sample size Methods Key findings Limitation
      Healthy individuals
       Brandwein et al. (2019) 822 skin samples 16S rRNA V4 sequencing Skin microbiome beta diversity and relative abundance of Corynebacterium positively correlated with BMI. BMI self-reported; cross-sectional design; no control for comorbidities; Specific skin area could not be identified
       Rood et al. (2018) 31 obese and 27 normal-weight pregnant women 16S rRNA V1-V3 sequencing In the mid-abdomen and Pfannenstiel area, obese individuals had higher levels of Firmicutes and Bacteroidetes, and lower levels of Actinobacteria compared to controls. Small sample size; pregnant women only (reduced generalizability); potential confounders (pregnancy-related factors, surgical prep. antibiotics) not fully controlled
       Vongsa et al. (2019) 20 women with high BMI (≥ 30), 20 with normal BMI 16S rRNA V1-V3 sequencing Women with normal BMI showed Lactobacillus-dominant flora; those with high BMI had more Finegoldia and Corynebacterium, particularly in the vulvar region. No significant differences were noted in abdominal skin. Limited to female subjects; region-specific sampling (vulvar/abdominal), potential confounders (ethnicity, diet, hygiene practices, and hormonal variation) were not fully adjusted.
       Walker et al. (2020) 10 obese (BMI 35–50) postmenopausal women, 10 normal-weight (BMI 18.5–26.9) women 16S rRNA V1-V3 sequencing Minimal differences in overall skin microbiome composition between groups (mid lower abdomen). Very small cohort; postmenopausal women only (reduced generalizability); potential confounders (ethnicity, diet, hygiene products, sexual activity, antibiotic history and hormonal variation) not fully adjusted.
       Ma et al. (2024) 198 healthy Chinese women 16S rRNA V3-V4 sequencing Higher BMI associated with impaired skin barrier (increased TEWL, decreased pH), increased bacterial and fungal diversity. Overweight group had elevated Streptococcus, Corynebacterium, Malassezia, Candida abundance. Significant correlations observed between skin physiology and microbial composition. Single anatomical site (face); cross-sectional design
      HS
       Haskin et al. (2016) 632 HS patients Bacterial culture of purulent drainage The odds of detecting Firmicutes were 3.1 times higher in obese HS patients than in non-obese counterparts. Culture-based (bias against unculturable bacteria); lack of control; potential confounders (antibiotic exposure and comorbidities) are not systematically controlled.
      Author Study design Sample size Intervention Key findings Limitation
      Psoriasis: Liraglutide
       Buysschaert et al. (2014) Prospective cohort 7 patients with type 2 DM and psoriasis 18 weeks of exenatide (5 μg BID) or liraglutide (1.2 mg daily) Mean PASI decreased from 12.0 to 9.2 Very small, uncontrolled case-series; Treatment & co-therapy heterogeneity; short follow-up
       Ahern et al. (2013) Prospective cohort 7 patients with type 2 DM and psoriasis 10 weeks of liraglutide (1.2 mg daily) Median PASI decreased from 4.8 to 3.0; DLQI from 6.0 to 2.0 Small open-label study without controls; low baseline disease activity; confounding by metabolic changes and co-therapies
      Faurschou et al. (2015) RCT 20 psoriasis patients 8 weeks of liraglutide (1.2 mg daily) vs. placebo No significant difference in PASI and DLQI between groups Small sample size and short treatment duration; no significant PASI/DLQI benefit over placebo
       Xu et al. (2019) Prospective cohort 7 patients with type 2 DM and psoriasis 12 weeks of liraglutide (1.2 mg daily) Mean PASI dropped from 15.7 to 2.2; DLQI from 21.6 to 4.1 Very small, uncontrolled study; short follow-up; potential confounders for metabolic and treatment regimens for diabetes
       Lin et al. (2022) RCT 25 psoriasis patients with type 2 DM 12 weeks of liraglutide vs. placebo Significant PASI improvement in treatment vs. control group Small, single-center, open-label trial; short follow-up; confounding by metabolic effects
      Psoriasis: Pioglitazone
       Singh and Bhansali et al. (2016) RCT 60 psoriasis patients with MS 12 weeks of pioglitazone vs. metformin vs. placebo Significant improvement in PASI, PGA, and ESI with pioglitazone and metformin Single center, open label study; short treatment window
       Ghiasi et al. (2019) RCT 60 psoriasis patients with MS 10 weeks of phototherapy + pioglitazone vs. phototherapy + placebo Greater PASI reduction in pioglitazone group Single center study; short treatment window; fixed-dose design
       Lajevardi et al. (2015) RCT 44 psoriasis patients 16 weeks of MTX + pioglitazone vs. MTX alone PASI75 achieved in 63.6% (combo) vs. 9.1% (MTX alone) Assessor-blinded only; single center trial with small sample size; male-predominant cohort
      HS: Liraglutide
       Nicolau et al. (2023) Prospective cohort 14 HS patients with obesity 12 weeks of liraglutide (3 mg) Significant reductions in BMI, Hurley stage, and DLQI Small sample size; short follow-up duration; lack of a control or placebo group
      Table 1. Summary of studies investigating the impact of obesity on skin microbiota

      Abbreviation: BMI, body mass index; HS, hidradenitis suppurativa; RNA, Ribonucleic acid.

      Table 2. Summary of longitudinal cohort studies and randomized controlled trials (RCTs) evaluating the effects of obesity-targeted pharmacologic interventions on psoriasis and hidradenitis suppurativa (HS)

      Abbreviation: DLQI, dermatology life quality index; DM, diabetes mellitus; ESI, erythema, scaling, and induration; MS, metabolic syndrome; MTX, methotrexate; PASI, psoriasis area and severity index; PGA, physician global assessment; RCT, randomized placebo-controlled trial.

      Table 1.

      Table 2.

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