Department of Food Science, National Taiwan Ocean University, 2, Pei-Ning Road, Keelung, Taiwan.
Biomaterials. 2013 Dec;34(38):10319-27. doi: 10.1016/j.biomaterials.2013.09.037. Epub 2013 Sep 27.
Methicillin-resistant Staphylococcus aureus (MRSA) causes infections through open skin injuries, and its resistance makes treatment difficult. The antimicrobial peptide Epinecidin-1 (Epi-1) has been reported to possess antibacterial, antifungal, antiviral, and antitumor functions. This study investigated the antimicrobial activity of Epi-1 against skin trauma-mediated MRSA infection in mice. One square centimeter of outer skin was excised from the ventral region of mice, and a lethal dose of MRSA was applied in the presence or absence of methicillin, vancomycin, or Epi-1. While untreated mice and mice treated with methicillin died within four days, mice treated with Epi-1 survived infection. Epi-1 decreased MRSA bacterial counts in the wounded region, enhanced wound closure, and increased angiogenesis at the injury site. Treatment with Epi-1 decreased serum levels of the proinflammatory cytokines TNF-α, IL-6, and MCP-1, and regulated the recruitment of monocytes and clearance of lymphocytes around the wounded region during healing. In conclusion, Epi-1 may be effective at treating clinical MRSA, and may enhance wound recovery when combined with collagen.
耐甲氧西林金黄色葡萄球菌（MRSA）可通过开放性皮肤损伤引起感染，其耐药性使得治疗变得困难。抗菌肽 Epinecidin-1（Epi-1）已被报道具有抗菌、抗真菌、抗病毒和抗肿瘤功能。本研究调查了 Epi-1 对小鼠皮肤创伤介导的 MRSA 感染的抗菌活性。从小鼠腹侧区域切除一平方厘米的外皮肤，并在存在或不存在甲氧西林、万古霉素或 Epi-1 的情况下应用致死剂量的 MRSA。未治疗的小鼠和用甲氧西林治疗的小鼠在四天内死亡，而用 Epi-1 治疗的小鼠则存活下来。Epi-1 降低了创伤部位的 MRSA 细菌数量，促进了伤口闭合，并增加了损伤部位的血管生成。Epi-1 治疗降低了血清中促炎细胞因子 TNF-α、IL-6 和 MCP-1 的水平，并在愈合过程中调节了单核细胞的募集和淋巴细胞在创伤区域的清除。总之，Epi-1 可能对治疗临床 MRSA 有效，并可能与胶原蛋白联合使用时增强伤口恢复。
