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Studies on the methods of nanoparticle (NP) synthesis, analysis of their characteristics, and exploration of new fields of their applications are at the forefront of modern nanotechnology. The possibility of engineering water-soluble NPs has paved the way to their use in various basic and applied biomedical researches. At present, NPs are used in diagnosis for imaging of numerous molecular markers of genetic and autoimmune diseases, malignant tumors, and many other disorders. NPs are also used for targeted delivery of drugs to tissues and organs, with controllable parameters of drug release and accumulation. In addition, there are examples of the use of NPs as active components, e.g., photosensitizers in photodynamic therapy and in hyperthermic tumor destruction through NP incorporation and heating. However, a high toxicity of NPs for living organisms is a strong limiting factor that hinders their use in vivo. Current studies on toxic effects of NPs aimed at identifying the targets and mechanisms of their harmful effects are carried out in cell culture models; studies on the patterns of NP transport, accumulation, degradation, and elimination, in animal models. This review systematizes and summarizes available data on how the mechanisms of NP toxicity for living systems are related to their physical and chemical properties.

Extracellular DNA trap formation is a cellular function of neutrophils, eosinophils, and basophils that facilitates the immobilization and killing of invading microorganisms in the extracellular milieu. To form extracellular traps, granulocytes release a scaffold consisting of mitochondrial DNA in association with granule proteins. As we understand more about the molecular mechanism for the formation of extracellular DNA traps, the in vivo function of this phenomenon under pathological conditions remains an enigma. In this article, we critically review the literature to summarize the evidence for extracellular DNA trap formation under in vivo conditions. Extracellular DNA traps have not only been detected in infectious diseases but also in chronic inflammatory diseases, as well as in cancer. While on the one hand, extracellular DNA traps clearly exhibit an important function in host defense, it appears that they can also contribute to the maintenance of inflammation and metastasis, suggesting that they may represent an interesting drug target for such pathological conditions.

Risk of severe coronavirus disease 2019 (COVID-19) after infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is increased in patients with certain comorbidities, including chronic obstructive pulmonary disease (COPD). By contrast, epidemiological data from many (but not all) countries indicate a low prevalence of asthma among patients with severe COVID-19. This reduced risk of severe COVID-19 may apply specifically to patients with the type 2 asthma endotype, which is most common in childhood asthma.Somewhat surprisingly, individuals with asthma do not seem to have a greater risk of developing severe COVID-19. Here, the authors offer mechanistic insights to explain the epidemiological data.

Eosinophils are specialized white blood cells, which are involved in the pathology of diverse allergic and nonallergic inflammatory diseases. Eosinophils are traditionally known as cytotoxic effector cells but have been suggested to additionally play a role in immunomodulation and maintenance of homeostasis. The exact role of these granule-containing leukocytes in health and diseases is still a matter of debate. Degranulation is one of the key effector functions of eosinophils in response to diverse stimuli. The different degranulation patterns occurring in eosinophils (piecemeal degranulation, exocytosis and cytolysis) have been extensively studied in the last few years. However, the exact mechanism of the diverse degranulation types remains unknown and is still under investigation. In this review, we focus on recent findings and highlight the diversity of stimulation and methods used to evaluate eosinophil degranulation.

Nano- and microparticles are increasingly widely used in biomedical research and applications, particularly as specific labels and targeted delivery vehicles. Silica has long been considered the best material for such vehicles, but it has some disadvantages limiting its potential, such as the proneness of silica-based carriers to spontaneous drug release. Calcium carbonate (CaCO3) is an emerging alternative, being an easily available, cost-effective, and biocompatible material with high porosity and surface reactivity, which makes it an attractive choice for targeted drug delivery. CaCO3 particles are used in this field in the form of either bare CaCO3 microbeads or core/shell microparticles representing polymer-coated CaCO3 cores. In addition, they serve as removable templates for obtaining hollow polymer microcapsules. Each of these types of particles has its specific advantages in terms of biomedical applications. CaCO3 microbeads are primarily used due to their capacity for carrying pharmaceutics, whereas core/shell systems ensure better protection of the drug-loaded core from the environment. Hollow polymer capsules are particularly attractive because they can encapsulate large amounts of pharmaceutical agents and can be so designed as to release their contents in the target site in response to specific stimuli. This review focuses first on the chemistry of the CaCO3 cores, core/shell microbeads, and polymer microcapsules. Then, systems using these structures for the delivery of therapeutic agents, including drugs, proteins, and DNA, are outlined. The results of the systematic analysis of available data are presented. They show that the encapsulation of various therapeutic agents in CaCO3-based microbeads or polymer microcapsules is a promising technique of drug delivery, especially in cancer therapy, enhancing drug bioavailability and specific targeting of cancer cells while reducing side effects. To date, research in CaCO3-based microparticles and polymer microcapsules assembled on CaCO3 templates has mainly dealt with their properties in vitro, whereas their in vivo behavior still remains poorly studied. However, the enormous potential of these highly biocompatible carriers for in vivo applications is undoubted. This last issue is addressed in depth in the Conclusions and Outlook sections of the review.

Engineered nano- and microparticles are considered as promising tools in biomedical applications, such as imaging, sensing, and drug delivery. Protein adsorption on these particles in biological media is an important factor affecting their properties, cellular interactions, and biological fate. Understanding the parameters determining the efficiency and pattern of protein adsorption is crucial for the development of effective biocompatible particle-based applications. This review focuses on the influence of the morphological and physicochemical properties of particles on protein adsorption, including the pattern and amount of the adsorbed protein species, as well as the relative abundance of proteins with specific functions or physicochemical parameters. The effects of functionalization of the particle surface with polyethylene glycol, zwitterions, zwitterionic polymers, or proteins on the subsequent protein adsorption are analyzed. In addition, the dependences of protein adsorption on the protein species, biological buffers, fluids, tissues, and other experimental conditions are looked into. The influence of protein adsorption on the targeting efficiency of particle-based delivery systems is also discussed. Finally, the effect of the adsorbed protein corona on the interaction of the engineered micro- and nanoparticles with cells and the roles of specific proteins adsorbed on the particle surface in the recognition of the particles by the immune system are considered.

Immunoglobulin E (IgE)-associated allergy is the most common immunologically-mediated hypersensensitivity disease. It is based on the production of IgE antibodies and T cell responses against innocuous antigens (i.e., allergens) and subsequent allergen-induced inflammation in genetically pre-disposed individuals. While allergen exposure in sensitized subjects mainly boosts IgE production and T cell activation, successful allergen-specific immunotherapy (AIT) induces the production of allergen-specific IgG antibodies and reduces T cell activity. Under both circumstances, the resulting allergen-antibody complexes play a major role in modulating secondary allergen-specific immune responses: Allergen-IgE complexes induce mast cell and basophil activation and perpetuate allergen-specific T cell responses via presentation of allergen by allergen presenting cells to T cells, a process called IgE-facilitated antigen presentation (FAP). In addition, they may induce activation of IgE memory B cells. Allergen-induced production of specific IgGs usually exerts ameliorating effects but under certain circumstances may also contribute to exacerbation. Allergen-specific IgG antibodies induced by AIT which compete with IgE for allergen binding (i.e., blocking IgG) inhibit formation of IgE-allergen complexes and reduce activation of effector cells, B cells and indirectly T cells as FAP is prevented. Experimental data provide evidence that by binding of allergen-specific IgG to epitopes different from those recognized by IgE, allergen-specific IgG may enhance IgE-mediated activation of mast cells, basophils and allergen-specific IgE B cells. In this review we provide an overview about the role of allergen-specific antibodies in regulating secondary allergen-specific immune responses.

Data on hereditary angioedema with normal C1 inhibitor levels are currently limited. To date, only one Italian family with HAE-MYOF has been described, comprising exclusively female members. The angioedema (AE) of head and neck area with the teenage onset, triggered by menses and high fever episodes were identified. It is necessary to search for potential biomarkers in patients with HAE-MYOF. This case series reports two unrelated individuals from different families with symptoms onset of recurrent AE and identified myoferlin gene mutations. Due to limited knowledge about the clinical presentation, pathogenesis, and treatment response in HAE-MYOF, further data collection is essential.

Autophagy is a highly conserved lysosomal degradation system that involves the creation of autophagosomes, which eventually fuse with lysosomes and breakdown misfolded proteins and damaged organelles with their enzymes. Autophagy is widely known for its function in cellular homeostasis under physiological and pathological settings. Defects in autophagy have been implicated in the pathophysiology of a variety of human diseases. The new line of evidence suggests that autophagy is inextricably linked to skin disorders. This review summarizes the principles behind autophagy and highlights current findings of autophagy’s role in skin disorders and strategies for therapeutic modulation.

Eosinophils are granule-containing leukocytes which develop in the bone marrow. For many years, eosinophils have been recognized as cytotoxic effector cells, but recent studies suggest that they perform additional immunomodulatory and homeostatic functions. Autophagy is a conserved intracellular process which preserves cellular homeostasis. Autophagy defects have been linked to the pathogenesis of many human disorders. Evidence for abnormal regulation of autophagy, including decreased or increased expression of autophagy-related (ATG) proteins, has been reported in several eosinophilic inflammatory disorders, such as Crohn’s disease, bronchial asthma, eosinophilic esophagitis, and chronic rhinosinusitis. Despite the increasing extent of research using preclinical models of immune cell-specific autophagy deficiency, the physiological relevance of autophagic pathway in eosinophils has remained unknown until recently. Owing to the increasing evidence that eosinophils play a role in keeping organismal homeostasis, the regulation of eosinophil functions is of considerable interest. Here, we discuss the most recent advances on the role of autophagy in eosinophils, placing particular emphasis on insights obtained in mouse models of infections and malignant diseases in which autophagy has genetically dismantled in the eosinophil lineage. These studies pointed to the possibility that autophagy-deficient eosinophils exaggerate inflammation. Therefore, the pharmacological modulation of the autophagic pathway in these cells could be used for therapeutic interventions.