The increasing incidence of hospital-acquired infections and antimicrobial-resistant pathogens poses a major clinical challenge. Nearly all medical devices are vulnerable to bacterial biofilm formation, which acts as a protective coating against the host defense systems and antibiotics. The persistence of biofilm infections, accounting for around 65% of all microbial infections, and poor conventional treatment outcomes has driven interest in alternative approaches like bacteriophage therapy. This review encompasses key aspects of biofilm biology, taking into account the clinically significant ESKAPE pathogens, and provides an in-depth analysis of the role of phage agents in biofilm control as a new biofilm control strategy. Diving deeper into the mechanisms of phage-mediated processes, the review examines how bacteriophages penetrate and disrupt biofilm architecture and evaluates current therapeutic strategies that exploit these actions, acknowledging their limitations and considering possible future directions.

The skin microbiome plays a pivotal role in maintaining skin homeostasis, immune regulation, and barrier integrity. Dysbiosis, characterized by altered diversity and function of the microflora, contributes to the pathogenesis of chronic inflammatory dermatoses such as atopic dermatitis, psoriasis, acne vulgaris, hidradenitis suppurativa, rosacea, and photoaging. This narrative review, based on searches in PubMed, Scopus, and Google Scholar, summarizes current evidence on the role of topical probiotics in the prevention and management of inflammatory dermatoses, drawing mainly on studies from the past decade and, where relevant, earlier works published between 1975 and 2025. Evidence indicates that topical probiotics modulate local immune responses, enhance antimicrobial peptide synthesis, inhibit pathogenic microorganism colonization, and support skin barrier regeneration. Additional benefits include accelerated wound healing and reduced environmental damage. However, study results are heterogeneous, and designs vary, with limited data on long-term effects, particularly in paediatric and immunosuppressed populations. Topical probiotics are a promising therapeutic approach for chronic inflammatory dermatoses linked to microbiota dysbiosis. They can restore microbial balance, support barrier function, suppress pathogenic microorganisms, and promote skin regeneration. Despite consistent reports of clinical improvement and improved cutaneous defence mechanisms, small sample sizes, methodological heterogeneity, and the absence of standardized dosing regimens limit current evidence. Long-term safety data are limited, especially for vulnerable patient groups. Rigorous randomized controlled trials with standardized protocols and larger, diverse populations are needed to confirm efficacy, ensure safety, and guide clinical implementation.

Antimicrobial resistance (AMR) represents a major global health threat, largely driven by antibiotic overuse and the protective role of bacterial biofilms. Quorum sensing (QS), a bacterial communication system regulating virulence and biofilm formation, has emerged as a promising therapeutic target. Quorum quenching (QQ), which disrupts QS without directly inhibiting bacterial growth, is considered a potential anti-virulence strategy that may reduce selective pressure for resistance. This review critically evaluates recent advances in QQ research, focusing on its clinical applicability, limitations, and risks. We analyzed studies from the last five years involving natural compounds, synthetic molecules, nanoparticles (NPs), and combination therapies targeting key pathogens such as Pseudomonas aeruginosa and Staphylococcus aureus in models of lung diseases, mainly cystic fibrosis, chronic wounds, burns, and implant-associated infections. While numerous compounds demonstrate significant in vitro anti-biofilm and anti-virulence activity, major challenges remain, including limited in vivo validation, pharmacokinetic constraints, toxicity concerns, microbiome disruption, and the potential development of tolerance or functional resistance. Although QQ offers a promising adjunctive approach to conventional antibiotics, its long-term clinical feasibility requires comprehensive evaluation of evolutionary dynamics, host–microbe interactions, and safety profiles.

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.

Rotavirus remains one of the leading causes of severe gastroenteritis, particularly among infants and young children, despite the introduction of effective vaccines. Although the global burden of rotavirus-associated morbidity and mortality has decreased in recent years, significant challenges remain regarding accurate diagnosis, optimal clinical management, and equitable access to preventive measures. The aim of this narrative review is to provide a comprehensive synthesis of recent advances in the diagnosis and treatment of rotavirus infections. Particular emphasis is placed on post-guideline research emerging after the publication of the Evidence-Based Guidelines from the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) and the European Society for Pediatric Infectious Diseases (ESPID), offering updated perspectives on therapeutic strategies and clinical practices. In addition, this review discusses the expanding role of molecular diagnostic methods, which offer enhanced sensitivity and specificity in the detection of rotavirus, and evaluates novel antiviral agents under investigation. By integrating and analyzing the most relevant research published within the past decade, we aim to delineate key progress, identify persistent gaps in knowledge, and propose future directions for research and clinical application.

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.