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Unfolding the physiological roles of the binding of Atl to eDNA in Staphylococcus aureus

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Staphylococcus aureus is usually a commensal organism of the human’s microbiota, although it can become invasive when the host’s defenses are breached, becoming an important nosocomial opportunistic pathogen, with high morbidity and mortality rates across the globe. It is responsible for a wide array of infections that range from minor skin and soft tissue infections to more severe ones, such as endocarditis, osteomyelitis and sepsis. This microorganism harbors a plethora of virulence factors that alongside its capacity to acquire resistance to virtually all antibiotics have enabled it to become one of the most prominent pathogens of this era. In fact, S. aureus is one of the major causes for infections associated with indwelling devices, which are usually related with biofilm development. Biofilms are multicellular sessile microbial communities in which cells are attached to a surface and/or to other cells and encased within a self-produced protective extracellular matrix. The biofilm forming capacity of S. aureus is part of the myriad of virulence mechanisms that enables this bacterium to resist both antibiotic treatment and the action of the host immune system.

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