Jett Bradley D, Gilmore Michael S
Department of Biology, Oklahoma Baptist University, Shawnee 74804, USA.
Infect Immun. 2002 Aug;70(8):4697-700. doi: 10.1128/IAI.70.8.4697-4700.2002.
Wild-type Staphylococcus aureus was observed to be capable of invading human corneal epithelial cells (HCEC) in vitro. Internalization of S. aureus required expression of fibronectin-binding proteins (FnBPs); the capacity of an FnBP-deficient isogenic strain to invade HCEC was reduced by more than 99%. The binding of S. aureus to HCEC did not require viable bacteria, since UV-killed cells were observed to adhere efficiently. Invasion of HCEC by S. aureus involved active host cell mechanisms; uptake was nearly completely eliminated by cytochalasin D and genistein. These data suggest that FnBPs play a key role in host-parasite interactions and may serve as an important adhesin or invasin in ulcerative keratitis caused by S. aureus.
观察到野生型金黄色葡萄球菌能够在体外侵入人角膜上皮细胞(HCEC)。金黄色葡萄球菌的内化需要纤连蛋白结合蛋白(FnBPs)的表达;一株FnBP缺陷的同基因菌株侵入HCEC的能力降低了99%以上。金黄色葡萄球菌与HCEC的结合不需要活细菌,因为观察到紫外线灭活的细胞能有效粘附。金黄色葡萄球菌对HCEC的侵入涉及宿主细胞的主动机制;细胞松弛素D和染料木黄酮几乎完全消除了摄取。这些数据表明FnBPs在宿主-寄生虫相互作用中起关键作用,并且可能是金黄色葡萄球菌引起的溃疡性角膜炎中的重要粘附素或侵袭素。