Role of extracellular vesicles as communication mediators between pathogens to potentiate pathogenicity in wound infections

金黄色葡萄球菌和铜绿假单胞菌的共同感染在慢性伤口患者中很常见，但对它们在细胞外囊泡（EVs）介导下的协同作用知之甚少。在这项研究中，我们研究了金黄色葡萄球菌（saev）和铜绿假单胞菌（paev）衍生的ev对其对应细菌致病性的影响。在2022财年，我们成功地从这两种病原体中分离和纯化了ev。研究了saev和paev对其对应细菌的影响，包括生长、抗生素耐药性、生物膜形成和致病性。我们发现paev抑制金黄色葡萄球菌的生长。相比之下，saev对铜绿假单胞菌的生长没有影响。由于paev抑制了金黄色葡萄球菌的生长，因此没有进行生物膜形成、抗生素耐药性和细胞感染等后续实验。我们发现saev并没有改变铜绿假单胞菌的耐药模式。有趣的是，经saev处理的铜绿假单胞菌比未经saev处理的铜绿假单胞菌有更高的生物膜形成。此外，saev还能增强人角化细胞对铜绿假单胞菌的侵袭。在进一步的研究中，我们将探讨saev促进铜绿假单胞菌生物膜形成和宿主细胞入侵的分子机制。此外，paev抑制金黄色葡萄球菌的机制也将进一步研究。

The co-infection of S. aureus and P. aeruginosa is common in patients with chronic wounds, but little is known about their synergistic effect mediated by extracellular vesicles (EVs). In this study, we investigate the effect of EVs derived from S. aureus (SaEVs) and P. aeruginosa (PaEVs) on the pathogenicity of their bacterial counterparts. In FY2022, we succeeded in the isolation and purification of the EVs from both pathogens. The effects of SaEVs, and PaEVs on their bacterial counterparts included growth, antibiotic resistance, biofilm formation, and pathogenicity were performed. We found that PaEVs inhibited the growth of S. aureus. In contrast, SaEVs did not have an effect on the growth of P. aeruginosa. Because of PaEVs inhibited S. aureus growth, the following experiments such as biofilm formation, antibiotic resistance, and cell infection were not investigated. We found SaEVs did not change the antibiotic-resistance pattern of P. aeruginosa. Interestingly, P. aeruginosa-treated with SaEVs had higher biofilm formation than non-treated P. aeruginosa with SaEVs. In addition, the SaEVs enhanced the human keratinocyte cell line’s invasion of P. aeruginosa. In a further study, we will investigate the molecular mechanisms of SaEVs to promote P. aeruginosa biofilm formation and host cell invasion. Furthermore, the mechanism by which PaEVs inhibit S. aureus will investigate.