Allergies

Background: Pruritus is burdensome across dermatoses. Beyond Staphylococcus, broader components of the cutaneous microbiome—bacteria, fungi, and viruses—and their products shape itch via barrier disruption, immune polarization, and direct neurosensory activation. Methods: We conducted a narrative review of human and translational studies. PubMed/MEDLINE, Scopus, and Web of Science were searched from inception to 27 August 2025 using terms for itch, skin microbiome, bacteriotherapy, proteases, PAR, TRP channels, IL-31, Malassezia, and AHR ligands. English and Italian records were screened; randomized trials, systematic reviews, and mechanistic studies were prioritized; and unsupported single case reports were excluded. Results: Beyond Staphylococcus aureus, microbial drivers include secreted proteases activating PAR-2/4; pore-forming peptides and toxins engaging MRGPRs and sensitizing TRPV1/TRPA1; and metabolites, especially tryptophan-derived AHR ligands, that recalibrate barrier and neuro-immune circuits. Commensal taxa can restore epidermal lipids, tight junctions, and antimicrobial peptides. Early studies of topical live biotherapeutics—Roseomonas mucosa and Staphylococcus hominis A9—report reductions in disease severity and itch. Fungal communities, particularly Malassezia, contribute via lipases and bioactive metabolites with context-dependent effects. Across studies, heterogeneous itch metrics, small samples, and short follow-up limit certainty. Conclusions: The cutaneous microbiome actively contributes to itch and is targetable. Future studies should prioritize standardized itch endpoints, responder stratification, and robust safety for live biotherapeutics.

Atopic dermatitis (AD) is a chronic inflammatory skin disease marked by pruritus and eczematous lesions that significantly impacts patient quality of life. This review covers the intricate interplay of barrier dysfunction, immune dysregulation, and microbial dysbiosis in the complex pathophysiology of AD. The roles of epigenetic factors and environmental exposures are also examined. The evolving understanding of these factors has revolutionized AD treatment. Beyond foundational topical agents, the landscape for moderate-to-severe AD treatment is now dominated by highly targeted immunotherapies, such as biologics and Janus Kinase (JAK) inhibitors, that precisely block specific inflammatory pathways. Emerging strategies explore microbiome modulation and vitamin D supplementation. This paradigm shift from broad immunosuppression to precision medicine offers improved disease control and reduced systemic toxicities and enables more personalized AD management, significantly benefiting patients.

Chronic rhinosinusitis (CRS) and allergic rhinitis (AR) are common comorbid sinonasal conditions. CRS is classically divided into two distinct phenotypes: CRS with nasal polyposis (CRSwNP) and CRS without nasal polyposis (CRSsNP). The purpose of this retrospective observational study is to determine whether aeroallergen sensitization profiles in patients with comorbid CRS and AR can distinguish between CRSwNP and CRSsNP. A total of 241 patients diagnosed with comorbid CRS and AR who underwent skin prick testing or in vitro allergy testing in a single tertiary rhinology practice were included for evaluation. The rates of allergen-specific sensitizations in CRSwNP patients were compared with those in CRSsNP patients. Of the allergens tested in the routine panels, Dermatophagoides pteronyssinus (OR = 1.82, p = 0.03), Alternaria (OR = 2.55, p < 0.01), and animal dander (OR = 1.48 for cat and OR = 3.01 for dog, p < 0.01) were predictive of CRSwNP. Sensitization to any grass allergen was also predictive of CRSwNP (OR = 2.09, p < 0.01). Multiple perennial aeroallergens showed strong associations with CRSwNP; however, broad sensitization to perennial allergens as a whole group was not significantly predictive of CRSwNP (OR = 1.83, p = 0.22).