Rotavirus (RV) is the most common cause of severe acute gastroenteritis (AGE) in children under five years of age. This review summarizes current knowledge on RV infections, with a particular focus on viral structure, pathophysiological mechanisms, and age-dependent clinical presentation. Special attention is given to systemic manifestations, including central nervous system involvement, autoimmune responses such as type 1 diabetes and celiac disease, and rare associations with biliary atresia. The mechanisms of RV-induced diarrhea and vomiting are discussed in detail. Clinical severity scoring systems—such as the Vesikari and Clark scales—and dehydration assessment tools—the Clinical Dehydration Scale (CDS) and the Dehydration: Assessing Kids Accurately (DHAKA) score—are compared. The review highlights differences in disease course between children under and over five years, emphasizing that RV is not limited to early childhood. A major section addresses the global effectiveness of vaccination programs, their role in reducing disease burden, coverage challenges, and decreased efficacy in low-income countries. Particular focus is placed on high-risk groups, including preterm and immunocompromised infants.

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.

Cutaneous warts caused by human papillomavirus (HPV) are among the most common dermatological conditions, affecting the quality of life of numerous people. Although they are widespread, effective and reliable treatment alternatives are limited, emphasizing the necessity for novel treatment options. Intralesional immunotherapy has emerged as a promising alternative, aiming to stimulate the host immune response to achieve the clearance of both treated and distant lesions. This review explores the immunopathogenesis of cutaneous warts and provides an in-depth analysis of intralesional therapies including measles–mumps–rubella (MMR) vaccine, purified protein derivative (PPD), Bacillus Calmette–Guérin (BCG), Candida antigen, Mycobacterium w vaccine (MWV), vitamin D3, and autoinoculation. We provide a comprehensive analysis of the most promising modalities, highlighting their mechanism of action, outcomes, advantages, and limitations. Although initial data indicate that intralesional immunotherapy offers advantageous efficacy and tolerability, there is a lack of standardized treatment protocols and randomized controlled trials to endorse its broad application. Nevertheless, considering its potential to address local and distant lesions with minimal adverse effects, intralesional immunotherapy may represent a transformative approach to managing cutaneous warts.

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.

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.