愛爾蘭科學(xué)家在5月出版的《微生物學(xué)》上撰文指出,，一種能與酵母菌進(jìn)行溝通的細(xì)菌可以抑制對藥物耐受酵母菌的感染,。這項(xiàng)研究為預(yù)防與醫(yī)學(xué)植入有關(guān)的醫(yī)院獲得性感染邁出了戰(zhàn)略性的一步。
愛爾蘭科克大學(xué)的研究人員對綠膿桿菌和白色念珠菌之間的相互影響進(jìn)行了研究,。綠膿桿菌與嚴(yán)重?zé)齻鸬母腥居嘘P(guān),，而白色念珠菌可以在諸如一些導(dǎo)管的塑料表面上生長。盡管這兩種微生物非常常見,，而且正常情況下對健康人也沒有危害,，但可以造成免疫功能低下者嚴(yán)重的感染。研究人員發(fā)現(xiàn),，綠膿桿菌所產(chǎn)生的一種分子能阻止白色念珠菌在硅膠導(dǎo)管表面的聚集生長,。有趣的是，這兩種微生物之間的相互作用不是依賴于叫做“群體感應(yīng)”的細(xì)菌通信系統(tǒng),。
白色念珠菌是最常見的醫(yī)院獲得性感染微生物,，它可以通過黏附在植入人體的塑料表面而引起疾病。這些塑料包括,，導(dǎo)管,、心臟裝置和人工關(guān)節(jié)等。生物膜的形成是白色念珠菌感染的關(guān)鍵,，同時(shí)也存在一個(gè)問題,，因?yàn)樯锬こ３χ委熕鼈兊乃幬锂a(chǎn)生耐受。領(lǐng)導(dǎo)這項(xiàng)研究的約翰莫里西博士說,，“白色念珠菌可以引起敏感患者嚴(yán)重的深部感染,，而且經(jīng)常會發(fā)現(xiàn)它們以生物膜形式存在。因此,，了解生物膜的形成過程以及如何去控制它非常重要,。”
莫里西認(rèn)為他的這項(xiàng)研究很有臨床意義。“如果我們能探索到一種與綠膿桿菌同樣的抑制方法，我們就能設(shè)計(jì)一種作為抗生素的藥物,，在生物膜形成后驅(qū)散它們,，或者作為塑料表面的添加劑防止生物膜在醫(yī)療植入體上的形成。”他說,。“下一步研究就是要找到綠膿桿菌所產(chǎn)生的這種化學(xué)物質(zhì)是什么,，以及這種物質(zhì)在白色念珠菌上的作用靶點(diǎn)，這樣我們就能知道開發(fā)一種用于臨床的藥物是否可行,。”（生物谷Bioon.com）
生物谷推薦原文出處：
Microbiology DOI：10.1099/mic.0.037549-0
Pseudomonas aeruginosa secreted factors impair biofilm development in Candida albicans
Lucy J. Holcombe1,, Gordon McAlester1,, Carol A. Munro3, Brice Enjalbert3, Alistair J. P. Brown3, Neil A. R. Gow3, Chen Ding4, Geraldine Butler4, Fergal O'Gara1,2 and John P. Morrissey1
1 Department of Microbiology, University College Cork, Cork, Ireland
2 BIOMERIT Research Centre, University College Cork, Cork, Ireland
3 Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK
4 School of Biomolecular and Biomedical Science, Conway Institute, University College Dublin, Dublin 4, Ireland
Signal-mediated interactions between the human opportunistic pathogens Pseudomonas aeruginosa and Candida albicans affect virulence traits in both organisms. Phenotypic studies revealed that bacterial supernatant from four P. aeruginosa strains strongly reduced the ability of C. albicans to form biofilms on silicone. This was largely a consequence of inhibition of biofilm maturation, a phenomenon also observed with supernatant prepared from non-clinical bacterial species. The effects of supernatant on biofilm formation were not mediated via interference with the yeast–hyphal morphological switch and occurred regardless of the level of homoserine lactone (HSL) produced, indicating that the effect is HSL-independent. A transcriptome analysis to dissect the effects of the P. aeruginosa supernatants on gene expression in the early stages of C. albicans biofilm formation identified 238 genes that exhibited reproducible changes in expression in response to all four supernatants. In particular, there was a strong increase in the expression of genes related to drug or toxin efflux and a decrease in expression of genes associated with adhesion and biofilm formation. Furthermore, expression of YWP1, which encodes a protein known to inhibit biofilm formation, was significantly increased. Biofilm formation is a key aspect of C. albicans infections, therefore the capacity of P. aeruginosa to antagonize this has clear biomedical implications.
