Ragweed (Ambrosia artemisiifolia) represents a major and expanding source of aeroallergen exposure in Europe, with rising sensitization rates and substantial clinical impact. However, population-level data integrating airborne pollen exposure with detailed clinical sensitization patterns remain limited. We conducted a 5-year retrospective cross-sectional observational analysis of sensitization prevalence, complemented by a parallel temporal analysis of aerobiological data and symptom-driven healthcare presentation patterns (2020–2024) in Timisoara, Romania, including all patients undergoing first-time sensitization evaluation at a tertiary referral hospital. Sensitization was assessed using standardized skin prick testing to common aeroallergens and other allergen categories, while airborne ragweed pollen concentrations were monitored through a peri-urban network of real-time bio-particle analyzers. Statistical analyses included descriptive statistics, multivariable logistic regression, χ² tests for co-sensitization patterns, and comparative analyses of clinical manifestations across sensitization profiles. Among 4404 eligible patients, 50.7% were sensitized to at least one allergen. Ragweed sensitization was identified in 24.1% of patients, with a mean age of 31.1 years at diagnosis and no significant sex-related difference. Most ragweed-sensitized patients were polysensitized (71.5%), predominantly to other aeroallergens. Increasing age was independently associated with lower odds of polysensitization to other aeroallergens (adjusted OR = 0.97 per year, 95% CI: 0.96–0.98), while sex showed no independent association. Patients with ragweed sensitization alone and those cosensitized with aeroallergens exhibited similar prevalence of respiratory manifestations, whereas individuals with additional non-aeroallergen sensitization showed lower prevalence of rhinitis, conjunctivitis, and asthma but slightly higher rates of asthma exacerbations. Weekly diagnoses of ragweed sensitization demonstrated a pronounced seasonal peak between calendar weeks 33 and 38 (mid-August to late September), coinciding with peak airborne ragweed pollen concentrations. Ragweed sensitization therefore represents a substantial and seasonally driven healthcare burden in western Romania, characterized by frequent polysensitization, distinct clinical manifestation patterns across sensitization profiles, and close temporal alignment between airborne pollen exposure and clinical presentation. Integrating aerobiological monitoring with clinical surveillance may support targeted prevention strategies and improved patient management.

Interleukin-11 (IL-11) is implicated in epithelial dysfunction, fibroblast activation, tissue remodeling, and chronic inflammatory responses; however, the clinical value of circulating IL-11 in airway disease remains uncertain. This single-center retrospective exploratory observational study included 88 adults: 31 with allergic rhinitis, 15 with non-allergic asthma, 22 with allergic asthma associated with allergic rhinitis, and 20 healthy controls. Serum IL-11 concentrations were measured using a quantitative sandwich enzyme-linked immunosorbent assay. Between-group differences were assessed using the Kruskal–Wallis test followed by Holm-adjusted pairwise Mann–Whitney U tests. Associations with disease-specific ordinal clinical categories were evaluated using Spearman rank correlation, with GINA treatment Steps used for asthma phenotypes and ARIA severity categories for allergic rhinitis. Median IL-11 concentrations were 62.01 pg/mL in non-allergic asthma, 78.87 pg/mL in allergic rhinitis, 61.92 pg/mL in allergic asthma associated with allergic rhinitis, and 95.46 pg/mL in healthy controls. The primary global comparison was not statistically significant (H = 5.667, p = 0.129), and no pairwise comparison remained significant after Holm correction. Six measurements (6.8%) were below the assay detection limit; replacing these values with 4.0 pg/mL in a sensitivity analysis did not materially alter the global result (H = 5.671, p = 0.129). Serum IL-11 was not significantly associated with GINA treatment step in non-allergic asthma (rho = −0.170, p = 0.544) or allergic asthma associated with allergic rhinitis (rho = 0.052, p = 0.818), nor with ARIA severity category in allergic rhinitis (rho = 0.046, p = 0.805). In an exploratory analysis adjusted for age, sex, body-mass category, and current smoking status, IL-11 concentrations were lower in each clinical phenotype relative to healthy controls; given the modest group sizes and baseline imbalance, this finding was considered hypothesis-generating. Overall, the primary analysis did not demonstrate significant differences in circulating IL-11 across study groups, and serum IL-11 was not associated with disease-specific ordinal clinical categories. These findings do not support the use of a single serum IL-11 measurement as a stand-alone biomarker of airway disease phenotype or clinical category in this cohort and warrant confirmation in larger, prospectively characterized cohorts.

Background/Objectives: Leptin is a pleiotropic adipokine linking energy metabolism with innate and adaptive immunity. Its relationship with clinical severity across distinct airway disease phenotypes remains insufficiently characterized. This study examined serum leptin concentrations in adults with allergic rhinitis, non-allergic asthma, and allergic asthma associated with allergic rhinitis. Methods: This single-center retrospective observational study analyzed fully anonymized clinical and laboratory data from 88 adults: patients with allergic rhinitis (n = 31), non-allergic asthma (n = 15), or allergic asthma with allergic rhinitis (n = 22) and healthy controls (n = 20). Serum leptin was measured using a quantitative sandwich enzyme-linked immunosorbent assay. Disease severity was classified using the Allergic Rhinitis and its Impact on Asthma and Global Initiative for Asthma frameworks applicable during the study period. Statistical analyses were performed using IBM SPSS Statistics, version 26.0 (IBM Corp., Armonk, NY, USA), and available original statistical outputs were summarized using retained t statistics and two-sided p values. Results: Stage-specific mean serum leptin concentrations were heterogeneous and non-monotonic. Statistically significant relationships between leptin concentration and disease stage were reported for allergic rhinitis (t = 2.844; p = 0.008), non-allergic asthma (t = 4.240; p = 0.001), and allergic asthma with allergic rhinitis (t = 2.700; p = 0.013). In the allergic rhinitis subgroup, 64.5% of participants had normal weight, 32.3% were overweight, and 3.2% had grade II obesity; weight category was not significantly related to rhinitis stage. Conclusions: The retained analyses indicate statistically significant relationships between serum leptin concentration and clinical disease stage across the investigated airway phenotypes. However, the stage-specific descriptive means were heterogeneous and non-monotonic and therefore do not support a uniform progressive increase in leptin with increasing disease severity. Because complete model outputs and covariate-adjusted estimates were unavailable, these findings should be regarded as exploratory and require prospective validation with appropriate adjustment for adiposity and other relevant metabolic confounders.

Background: Interleukin-17 (IL-17) contributes to persistent airway inflammation, neutrophil recruitment, and inflammatory pathways extending beyond classical type 2 immunity. However, the distribution of circulating IL-17 across clinically distinct upper- and lower-airway disease phenotypes remains incompletely characterized. This study compared serum IL-17 concentrations in allergic rhinitis, non-allergic asthma, allergic asthma associated with allergic rhinitis, and healthy controls. Methods: This retrospective single-center observational study included 88 adults: allergic rhinitis (n = 31), non-allergic asthma (n = 15), allergic asthma associated with allergic rhinitis (n = 22), and healthy controls (n = 20). Serum IL-17 concentrations were measured using a quantitative sandwich enzyme-linked immunosorbent assay. Overall group differences were assessed using the Kruskal–Wallis test, followed by Holm-adjusted pairwise Mann–Whitney U tests. Results: Serum IL-17 concentrations differed significantly across the four groups (Kruskal–Wallis H = 12.981, p = 0.0047). Median IL-17 concentrations were 126.21 pg/mL in non-allergic asthma, 50.97 pg/mL in allergic rhinitis, 54.72 pg/mL in allergic asthma associated with allergic rhinitis, and 0.00 pg/mL in healthy controls. Each disease group had significantly higher IL-17 than controls after Holm correction (adjusted p = 0.0103, 0.0172, and 0.0196, respectively), whereas the three disease phenotypes did not differ significantly from one another. Conclusions: Circulating IL-17 concentrations were higher in allergic rhinitis, non-allergic asthma, and allergic asthma associated with allergic rhinitis than in healthy controls. However, the substantial overlap among disease phenotypes and the absence of statistically significant between-phenotype differences should not be interpreted as evidence of equivalence or a shared biological mechanism. These findings should be considered exploratory and require confirmation in larger, prospectively characterized cohorts.

Chronic wounds represent a growing global healthcare burden driven by persistent inflammation, polymicrobial biofilm formation, impaired tissue regeneration, and increased antimicrobial resistance. This review examines the mechanistic interplay between chronic wound pathophysiology, biofilm persistence, and antimicrobial peptide (AMP)-based therapeutics, with particular emphasis on translational barriers and advanced biomaterial-enabled delivery strategies. Current evidence demonstrates that AMPs exert multifactorial activities extending beyond direct antimicrobial effects, including membrane disruption, quorum-sensing inhibition, extracellular polymeric substance (EPS) destabilization, immune modulation, angiogenic stimulation, and promotion of re-epithelialization. However, their clinical translation remains limited due to proteolytic degradation, poor stability, cytotoxicity, rapid clearance, and inadequate retention within the hostile chronic wound microenvironment. To address these limitations, emerging biomaterial platforms—including hydrogels, electrospun nanofibers, nanoparticles, self-assembling peptide systems, and stimuli-responsive smart dressings—have been developed to improve AMP stability, controlled release, biofilm penetration, and regenerative efficacy. This review further highlights current preclinical and clinical challenges, including the lack of standardized polymicrobial biofilm models and translationally relevant wound systems, while discussing future perspectives such as artificial intelligence-assisted peptide design and precision wound therapeutics. We argue that peptide discovery is no longer the principal bottleneck: the rate-limiting steps are now peptide stabilization, biofilm-targeted delivery, and dosing, and no current platform yet couples validated eradication of mature polymicrobial biofilms with validated tissue regeneration in a clinically representative model. Collectively, AMP-enabled smart biomaterials may support the transition from passive wound management toward responsive, biofilm-targeted regenerative therapy.

Chia seed (Salvia hispanica L.) is increasingly incorporated into contemporary foods, yet its allergenic potential remains poorly characterized. Published clinical evidence is limited to a small number of case reports, conference reports, and one case series describing immediate IgE-mediated reactions, cutaneous manifestations, and anaphylaxis. Molecular studies have identified candidate allergenic protein families, including 2S albumins, 7S vicilin-like globulins, 11S legumin-like globulins, and oleosins, and have demonstrated IgE recognition and potential cross-reactivity, particularly with sesame. However, molecular cross-recognition does not establish clinically relevant cross-allergy. This structured narrative review synthesizes the available clinical and molecular evidence regarding chia seed allergy, with emphasis on clinical manifestations, candidate allergens, chia–sesame cross-reactivity, diagnosis, and major knowledge gaps. Current evidence supports chia as a potential emerging food allergen but is insufficient to determine prevalence, natural history, reaction thresholds, or individual risk. Standardized diagnostic extracts, validated specific IgE thresholds, component-resolved diagnostics, and chia-specific oral food challenge protocols are currently lacking. Prospective clinical studies and further molecular characterization are required to establish the true clinical significance of chia seed allergy.