AAC：药物埃索美拉唑可明显抑制致病菌引发的生物被膜感染

近日，国际著名杂志<em>Antimicrobial Agents and Chemotherapy</em>在线刊登了美国休斯敦大学的研究者的最新研究成果“Inhibition of Biofilm Formation by Esomeprazole in <em>Pseudomonas aeruginosa</em> and <em>Staphylococcus aureus</em>”，文章中，研究者揭示了消化系统药物埃索美拉唑（Esomeprazole）如何抑制绿脓杆菌和金黄色葡萄球菌的生物被膜形成。

金黄色葡萄球菌（<em>Staphylococcus aureus</em>）和绿脓杆菌（<em>Pseudomonas aeruginosa</em>）是常见的院内致病菌，这两种细菌常常可引发生物被膜相关的感染性疾病。

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绿脓杆菌，又称铜绿假单胞菌是一种革兰氏阴性机会致病菌，也是一种一种令免疫受损的机会性感染病原，常常影响肺部及泌尿道，或造成烧伤、伤口及其他血液感染，如败血病和肺部纤维囊肿化等。然而金黄色葡萄球菌为一种革兰氏染色阳性球型细菌。是常见的引起食物中毒的致病菌，该菌可引起不同程度的化脓性炎症扩散疾病，如中耳炎、鼻窦炎骨髓炎、脓毒病等。在美国每年有几百万人会不同程度地感染这两种致病菌。

质子泵抑制剂（PPI）比如药物埃索美拉唑（Esomeprazole）或许会成为新型的抗致病菌制剂。研究者Kevin表示，这项研究就是来评估是否埃索美拉唑可以阻止细菌的生长以及生物被膜的形成，而且其是否可以和标准抗生素联合具有杀伤效应。

研究报告中，研究者检测了0.25mM的埃索美拉唑抵御金黄色葡萄球菌和绿脓杆菌生物被膜生成的效应。研究者使用96孔板来检测这两种细菌在药物埃索美拉唑作用下的CFU和生物量（生物被膜）的生成，检测时间为72小时。72小时完成后，研究者在随后的24小时内，检测了在埃索美拉唑中添加万古霉素（针对金黄色葡萄球菌）和添加美洛培南（针对绿脓杆菌）时候细菌的CFU和生物量。

暴露于药物埃索美拉唑中，两种细菌的生物被膜均发生了明显的降低，相比对照组（只暴露于一般的抗生素），加入埃索美拉唑后，两种细菌的杀伤效力大大增加，而且生物量也大大降低。而且随后的24小时测定结果显示，在抗生素和药物的作用下，两种细菌的生物被膜产生量也发生了明显降低。因此，研究者总结道，药物埃索美拉唑可以抵御绿脓杆菌和金黄色葡萄球菌产生生物被膜，可以有效阻止其生物被膜相关的疾病感染，或许会成为未来的一个新型的抗生素制剂。 
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<a title="" href="http://dx.doi.org/doi:10.1128/AAC.00544-12" target="_blank">doi:10.1128/AAC.00544-12</a>
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<br/><strong>Inhibition of Biofilm Formation by Esomeprazole in Pseudomonas aeruginosa and Staphylococcus aureus</strong><br/>


Vandana Singh, Vaneet Arora, M. Jahangir Alam and Kevin W. Garey

Staphylococcus aureus and Pseudomonas aeruginosa are common nosocomial pathogens responsible for biofilm-associated infections. Proton pump inhibitors (PPI), such as esomeprazole, may have novel antimicrobial properties. The objective of this study was to assess whether esomeprazole prevents sessile bacterial growth and biofilm formation and whether it may have synergistic killing effects with standard antibiotics. The antibiofilm activity of esomeprazole at 0.25 mM was tested against two strains each of S. aureus and P. aeruginosa. Bacterial biofilms were prepared using a commercially available 96-peg-plate Calgary biofilm device. Sessile bacterial CFU counts and biomass were assessed during 72 hours of esomeprazole exposure. The killing activities after an additional 24 hours of vancomycin (against S. aureus) and meropenem (against P. aeruginosa) treatment with or without preexposure to esomeprazole were also assessed by CFU and biomass analyses. P. aeruginosa and S. aureus strains exposed to esomeprazole displayed decreased sessile bacterial growth and biomass (P &lt; 0.001, each parameter). After 72 h of exposure, there was a 1-log10 decrease in the CFU/ml of esomeprazole-exposed P. aeruginosa and S. aureus strains compared to controls (P &lt; 0.001). After 72 h of exposure, measured absorbance was 100% greater in P. aeruginosa control strains than in esomeprazole-exposed strains (P &lt; 0.001). Increased killing and decreased biomass were observed for esomeprazole-treated bacteria compared to untreated controls exposed to conventional antibiotics (P &lt; 0.001, each parameter). Reduced biofilm growth after 24 h was visibly apparent by light micrographs for P. aeruginosa and S. aureus isolates exposed to esomeprazole compared to untreated controls. In conclusion, esomeprazole demonstrated an antibiofilm effect against biofilm-producing S. aureus and P. aeruginosa.

<br/>来源：生物谷

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