Chronic inflammatory skin diseases such as atopic dermatitis, psoriasis, and hidradenitis suppurativa are systemic conditions marked by persistent immune activation. Growing evidence links them to molecular and vascular ageing, including oxidative stress, endothelial dysfunction, and reduced expression of longevity-related proteins like Klotho and SIRT1. This narrative review examines how Th17- and Th2-driven inflammation contributes to systemic inflammageing. Key cytokines—IL-17, IL-23, IL-4, IL-13, and IL-31—promote endothelial damage, oxidative stress, and metabolic dysfunction. We highlight the role of vascular biomarkers (e.g., VCAM-1, ICAM-1, ST2, P-selectin) and immune cell senescence as indicators of ageing. Finally, we explore whether biologic therapies targeting these pathways may attenuate inflammation-driven ageing. Chronic skin diseases may thus serve as accessible models of systemic inflammageing and targets for early intervention.

Chronic inflammatory skin diseases, including atopic dermatitis (AD) and psoriasis, are systemic immune-mediated disorders driven by dysregulated immune responses. The gut–skin axis is a bidirectional network linking intestinal microorganisms, their metabolites, and host immunity. It connects microbiome composition and function with systemic inflammation and cutaneous pathology, shaping disease-specific mechanisms such as Th2/IL-4/IL-13-mediated barrier dysfunction in AD and Th17/IL-23/IL-17-driven hyperproliferation in psoriasis. Microbiota-derived metabolites, including short-chain fatty acids, tryptophan-derived aryl hydrocarbon receptor ligands, and bile acid-dependent FXR/TGR5 signaling, modulate immune homeostasis and epithelial integrity. Gut dysbiosis, impaired metabolite production, and barrier dysfunction disrupt regulatory networks, amplifying inflammation. Microbiota-targeted interventions, including probiotics, synbiotics, postbiotics, and precision nutrition, may serve as adjunctive therapies, although further well-controlled clinical studies are needed. Integrating multi-omics, metabolomics, and functional microbial profiling, alongside investigations of the gut mycobiome and virome, will be critical to identify predictive biomarkers and optimize therapeutic strategies. These concepts remain mechanistically compelling but largely theoretical, requiring validation in longitudinal and interventional studies.

Chronic inflammatory skin diseases, including psoriasis, hidradenitis suppurativa (HS), and atopic dermatitis (AD), are increasingly recognized as systemic disorders associated with chronic immune dysregulation. Growing evidence supports their links with metabolic disorders, reflected in heightened interest in therapeutic strategies targeting the immunometabolic axis. This review summarizes current knowledge on the role of glucagon-like peptide-1 receptor agonists (GLP-1RAs) in the regulation of immune and metabolic processes in chronic inflammatory skin diseases, with particular emphasis on molecular mechanisms and available experimental and clinical data. GLP-1RAs, widely used in the treatment of type 2 diabetes and obesity, may also exhibit anti-inflammatory and immunomodulatory properties beyond their classical metabolic effects. GLP-1 signalling can influence keratinocyte function, immune cell activity, and wound healing. Furthermore, it modulates multiple intracellular signalling pathways, including cAMP/PKA, AMPK, PI3K/Akt, and NF-κB, as well as immune axes such as IL-23/Th17/IL-17 and inflammasome-related signalling. Available evidence suggests that GLP-1RAs may reduce inflammation and disease activity in selected inflammatory dermatoses. However, current evidence remains limited and is based primarily on experimental studies, case reports, and small-scale observational studies. Further well-designed clinical trials are needed to better define the therapeutic potential of GLP-1RAs and their role in dermatological practice.

Introduction: Water quality is a critical issue affecting human health, with contamination by pathogens leading to various diseases. Pathogens in water, often transmitted through the fecal-oral route, pose significant risks, causing gastrointestinal diseases and bacterial diarrhea. The World Health Organization (WHO) has set water quality standards for recreational use, and sports events like triathlons and the Olympics may involve waterborne infection risks. Additionally, athletes in water sports face health risks from physical exertion and environmental conditions, including exercise-induced bronchoconstriction, hypothermia, hyperthermia and swimming-induced pulmonary edema. Understanding these risks and implementing preventive measures are crucial for ensuring the safety and health of athletes and participants in water-based sports events. Purpose of the work: The purpose of this study is to review the impact and risks of pathogenic microorganisms found in water on the health and physical performance of athletes. Special attention is given to the organization of water sports competitions in the context of microbiological threats. Materials and methods: A comprehensive analysis of research articles available on PubMed, Google Scholar, Web of Science, Embase, and Scopus was conducted using search terms related to: "water sports", "microbiological hazards", "water pathogens", "water quality", "athletes" and "prevention." Results: Microbiological threats included in water expose participants in major sporting events to potential infection that can cause various health issues. To reduce these risks, water quality standards must be monitored, and actions should be taken when limits are exceeded. Event organizers must prioritize athlete safety, considering factors like weather and water quality, and involve public health authorities in decision-making. If health risks are identified, rescheduling or changing the event location should be considered.

Psoriasis is a chronic, immune-mediated inflammatory skin disease requiring effective long-term systemic treatment. Current options, including using conventional small molecules and biological therapies, are limited by adverse events, suboptimal efficacy, or poor adherence due to inconvenient administration. This highlights an unmet need for safe, convenient, and effective oral self-administered dosage form therapies aligned with patient preferences. This review evaluates the mechanism, safety, and efficacy of next-generation tyrosine kinase 2 (TYK2) inhibitors and compares them to currently available therapeutic options. The pathogenesis of psoriasis is driven by chronic systemic inflammation mediated by the interleukin-23 (IL-23)/Th17/interleukin-17 (IL-17) axis. Selective TYK2 inhibitors, such as deucravacitinib, envudeucitinib, and zasocitinib, act through a unique allosteric mechanism by binding to the regulatory pseudokinase domain (JH2) rather than the enzyme’s catalytic domain. This enables highly selective suppression of IL-23-mediated inflammation while mitigating systemic toxicity seen with nonselective Janus kinase (JAK) inhibitors. Clinical trials (POETYK PSO-1 and PSO-2) and long-term extension studies demonstrate that deucravacitinib provides superior efficacy compared to the first-generation oral small molecule apremilast, with high and sustained response rates. It maintains durable efficacy for up to four years in patients with moderate to severe plaque psoriasis and shows a stable long-term safety profile, with low incidence of major adverse cardiovascular events (MACEs), venous thromboembolism (VTE), serious infections, and malignancies. Selective TYK2 inhibition bridges the therapeutic gap, providing an optimal balance of efficacy and oral convenience. With the potential to improve patient adherence and quality of life, these agents represent a promising option to become a first-line oral systemic therapy for psoriasis.

Iron deficiency (ID) has emerged as a pivotal yet underrecognized factor in the pathogenesis of immune-mediated inflammatory skin diseases (IMISDs) such as psoriasis, atopic dermatitis, and hidradenitis suppurativa. Beyond its classical role in erythropoiesis, iron acts as a key modulator of immune cell activity, redox balance, and overall metabolic homeostasis. This review synthesises the latest evidence on the intricate relationship between systemic inflammation, disturbances of iron metabolism, and immunometabolic imbalances that underline the pathogenesis of IMISDs. Findings indicate that chronic inflammation drives functional iron deficiency through IL-6–hepcidin-mediated sequestration of iron, resulting in reduced bioavailability and altered mitochondrial activity in immune and epithelial cells. This imbalance is associated with excessive and chronically enhanced oxidative and inflammatory responses of these cells, further advancing inflammation, anaemia of chronic disease, and disturbances of tissue repair. Moreover, emerging evidence supports an “iron-skin axis,” and suggests that skin cells, particularly epidermal keratinocytes, are actively involved in the regulation of iron pathways. Collectively, these insights position iron homeostasis as a missing link between systemic inflammation, immunometabolic imbalance, and disease burden in IMISDs.