| Summary: | Atopic dermatitis (AD) is a chronic and relapsing inflammatory cutaneous disease. The role of host defense and microbial virulence factors in <i>Staphylococcus aureus</i> skin colonization, infection, and inflammation perpetuation in AD remains an area of current research focus. Extracellular vesicles (EV) mediate cell-to-cell communication by transporting and delivering bioactive molecules, such as nucleic acids, proteins, and enzymes, to recipient cells. <i>Staphylococcus aureus</i> spontaneously secretes extracellular vesicles (SA-derived EVs)<i>,</i> which spread throughout the skin layers. Previous research has shown that SA-derived EVs from AD patients can trigger cytokine secretion in keratinocytes, shape the recruitment of neutrophils and monocytes, and induce inflammatory AD-type lesions in mouse models, in addition to their role as exogenous worsening factors for the disease. In this review article, we aim to examine the role of SA-derived EVs in AD physiopathology and its progression, highlighting the recent research in the field and exploring the potential crosstalk between the host and the microbiota.
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