Gamma rays and electrons with kinetic energy up to 10 MeV are routinely used to sterilize biomaterials. To date, the effects of irradiation upon human acellular dermal matrices (hADMs) remain to be fully elucidated. The optimal irradiation dosage remains a critical parameter affecting the final product structure and, by extension, its therapeutic potential. ADM slides were prepared by various digestion methods. The influence of various doses of radiation sterilization using a high-energy electron beam on the structure of collagen, the formation of free radicals and immune responses to non-irradiated (native) and irradiated hADM was investigated. The study of the structure changes was carried out using the following methods: immunohistology, immunoblotting, and electron paramagnetic resonance (EPR) spectroscopy. It was shown that radiation sterilization did not change the architecture and three-dimensional structure of hADM; however, it significantly influenced the degradation of collagen fibers and induced the production of free radicals in a dose-dependent manner. More importantly, the observed effects did not disrupt the therapeutic potential of the new transplants. Therefore, radiation sterilization at a dose of 35kGy can ensure high sterility of the dressing while maintaining its therapeutic potential.

The management of hard-to-heal wounds is a significant clinical challenge. Acellular dermal matrices (ADMs) have been successfully introduced to enhance the healing process. Here, we aimed to develop protocol for the preparation of novel ADMs from abdominoplasty skin. We used three different decellularization protocols for skin processing, namely, 1M NaCl and sodium dodecyl sulfate (SDS, in ADM1); 2M NaCl and sodium dodecyl sulfate (SDS, in ADM1); and a combination of recombinant trypsin and Triton X-100 (in hADM 3). We assessed the effectiveness of decellularization and ADM’s structure by using histochemical and immunochemical staining. In addition, we evaluated the therapeutic potential of novel ADMs in a murine model of wound healing. Furthermore, targeted transcriptomic profiling of genes associated with wound healing was performed. First, we found that all three proposed methods of decellularization effectively removed cellular components from abdominoplasty skin. We showed, however, significant differences in the presence of class I human leukocyte antigen (HLA class I ABC), Talin 1/2, and chondroitin sulfate proteoglycan (NG2). In addition, we found that protocols, when utilized differentially, influenced the preservation of types I, III, IV, and VII collagens. Finally, we showed that abdominoplasty skin-derived ADMs might serve as an effective and safe option for deep wound treatment. More importantly, our novel dressing (ADM1) improves the kinetics of wound closure and scar maturation in the proliferative and remodeling phases of wound healing. In conclusion, we developed a protocol for abdominoplasty skin decellularization suitable for the preparation of biological dressings. We showed that different decellularization methods affect the purity, structure, and therapeutic properties of ADMs.

Asthma is a complex airway disorder driven by diverse immunological pathways. While type 2 (T2)‐mediated inflammation is well characterized, the mechanisms underlying T2‐low (also referred to as mixed inflammatory phenotype) or non‐T2‐mediated asthma, often associated with Th1/Th17‐driven immune responses and high pulmonary neutrophilic inflammation, remain poorly understood. This study investigates airway remodeling in acute and chronic experimental asthma models induced by house dust mite extract to elucidate inflammatory and structural changes. Two acute T2‐low models demonstrated pronounced airway inflammation characterized by goblet cell hyperplasia, collagen deposition, and significant upregulation of extracellular matrix remodeling and fibroblast activation. In contrast, the chronic Th17‐mediated model exhibited reduced ECM deposition, increased matrix metalloproteinase (MMP) activity, and a distinct molecular signature dominated by IL‐17A‐driven pathways, indicative of ECM degradation and structural instability. Furthermore, the acute models showed immune cell apoptosis as the predominant cell death mechanism. In contrast, the chronic inflammation model was marked by necroptosis localized to structural lung cells, contributing to persistent inflammation and remodeling. Our findings provide new insights into the distinct immunopathological mechanisms underlying airway remodeling and fibrosis in T2‐low and Th17‐mediated asthma phenotypes. The study emphasizes the need for advanced preclinical models and targeted therapeutic strategies to address ECM dysregulation and chronic inflammation to progress in airway remodeling treatment in asthma.

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Background: The exact role of individual inflammatory factor in heart failure with reduced ejection fraction (HFrEF) remains elusive. The study aimed to evaluate three monocyte subsets (classical-CD14⁺⁺CD16⁻, intermediate-CD14⁺⁺CD16⁺, and nonclassical-CD14⁺CD16⁺⁺) in HFrEF patients and to assess the effect of the cardiac resynchronization therapy (CRT) on the changes in monocyte compartment. Methods: The study included 85 patients with stable HFrEF. Twenty-five of them underwent CRT device implantation with subsequent 6-month assessment. The control group consisted of 23 volunteers without HFrEF. Results: The analysis revealed that frequencies of non-classical-CD14⁺CD16⁺⁺ monocytes were lower in HFrEF patients compared to the control group (6.98 IQR: 4.95–8.65 vs. 8.37 IQR: 6.47–9.94; p = 0.021), while CD14⁺⁺CD16⁺ and CD14⁺⁺CD16⁻ did not differ. The analysis effect of CRT on the frequency of analysed monocyte subsets 6 months after CRT device implantation showed a significant increase in CD14⁺CD16⁺⁺ (from 7 IQR: 4.5–8.4 to 7.9 IQR: 6.5–9.5; p = 0.042) and CD14⁺⁺CD16⁺ (from 5.1 IQR: 3.7–6.5 to 6.8 IQR: 5.4–7.4; p = 0.017) monocytes, while the frequency of steady-state CD14⁺⁺CD16⁻ monocytes was decreased (from 81.4 IQR: 78–86.2 to 78.2 IQR: 76.1–81.7; p = 0.003). Conclusions: HFrEF patients present altered monocyte composition. CRT-related changes in the monocyte compartment achieve levels observed in controls without HFrEF.