Irene Magnifico

Living organisms must adapt and communicate effectively in their environment to survive. Cells communicate through various mechanisms, including releasing growth factors, chemokines, small bioactive molecules, and cell–cell contact. In recent years, a new and sophisticated cell communication mechanism based on extracellular vesicles (EVs) has been described in all three domains of life: archaea, bacteria, and eukaryotes. EVs are small, bilayer proteolipid vesicles released by cells into the extracellular space. This review aims to analyze and compare the current literature on bacterial, archaeal, and eukaryotic EVs and their possible clinical applications. This framework will address three key points: (a) The role of EVs in bacteria, eukaryotes, and archaea. (b) What is the impact of EVs in archaea on disease? (c) How archaea use EVs to communicate with other domains (bacteria/eukaryotes).

Long-term inflammatory skin disease atopic dermatitis is characterized by dry skin, itching, and eczematous lesions. During inflammation skin barrier protein impairment promotes S. aureus colonisation in the inflamed skin, worsening AD patient’s clinical condition. Proteomic analysis revealed the presence of several immune evasion proteins and virulence factors in S. aureus extracellular vesicles (EVs), suggesting a possible role for these proteins in the pathophysiology of atopic dermatitis. The objective of this study is to assess the efficacy of a wall fragment obtained from a patented strain of C. acnes DSM28251 (c40) and its combination with a mucopolysaccharide carrier (HAc40) in counteract the pathogenic potential of EVs produced by S. aureus ATCC 14458. Results obtained from in vitro studies on HaCaT keratinocyte cells showed that HAc40 and c40 treatment significantly altered the size and pathogenicity of S. aureus EVs. Specifically, EVs grew larger, potentially reducing their ability to interact with the target cells and decreasing cytotoxicity. Additionally, the overexpression of the tight junctions mRNA zona occludens 1 (ZO1) and claudin 1 (CLDN1) following EVs exposure was decreased by HAc40 and c40 treatment, indicating a protective effect on the epidermal barrier’s function. These findings demonstrate how Hac40 and c40 may mitigate the harmful effects of S. aureus EVs. Further investigation is needed to elucidate the exact mechanisms underlying this interaction and explore the potential clinical utility of c40 and its mucopolysaccharide carrier conjugate HAc40 in managing atopic dermatitis.