Darby Creg
Department of Cell and Tissue Biology, University of California, San Francisco, Box 0640/Room C-734, San Francisco, CA 94143-0640, USA.
Trends Microbiol. 2008 Apr;16(4):158-64. doi: 10.1016/j.tim.2008.01.005. Epub 2008 Mar 14.
Bubonic plague, one of history's deadliest infections, is transmitted by fleas infected with Yersinia pestis. The bacteria can starve fleas by blocking their digestive tracts, which stimulates the insects to bite repeatedly and thereby infect new hosts. Direct examination of infected fleas, aided by in vitro studies and experiments with the nematode Caenorhabditis elegans, have established that Y. pestis forms a biofilm in the insect. The extracellular matrix of the biofilm seems to contain a homopolymer of N-acetyl-d-glucosamine, which is a constituent of many bacterial biofilms. A regulatory mechanism involved in Y. pestis biofilm formation, cyclic-di-GMP signaling, is also widespread in bacteria; yet only Y. pestis forms biofilms in fleas. Here, the historical background of bubonic plague is briefly described and recent studies investigating the mechanisms by which these unique and deadly biofilms are formed are discussed.
腺鼠疫是历史上最致命的传染病之一,由感染鼠疫耶尔森菌的跳蚤传播。这种细菌会阻塞跳蚤的消化道,使其挨饿,从而刺激跳蚤反复叮咬,进而感染新的宿主。借助体外研究以及对线虫秀丽隐杆线虫的实验,对受感染跳蚤的直接检查证实,鼠疫耶尔森菌在昆虫体内形成了生物膜。生物膜的细胞外基质似乎含有N-乙酰-D-葡萄糖胺的同聚物,这是许多细菌生物膜的一种成分。参与鼠疫耶尔森菌生物膜形成的一种调节机制——环二鸟苷信号传导,在细菌中也很普遍;然而,只有鼠疫耶尔森菌会在跳蚤体内形成生物膜。在此,简要介绍腺鼠疫的历史背景,并讨论最近关于这些独特而致命的生物膜形成机制的研究。