Papp-Wallace Krisztina M, Maguire Michael E
Department of Pharmacology, Case Western Reserve University, Cleveland, Ohio 44106-4965, USA.
Annu Rev Microbiol. 2006;60:187-209. doi: 10.1146/annurev.micro.60.080805.142149.
Two areas of research have recently converged to highlight important roles for Mn(2+) in pathogenesis: the recognition that both bacterial Nramp homologs and members of LraI family of proteins are Mn(2+) transporters. Their mutation is associated with decreased virulence of various bacterial species. Thus, Mn(2+) appears to be essential for bacterial virulence. This review describes what is currently known about Mn(2+) transport in prokaryotes and how prokaryotic Mn(2+) transport is regulated. Some of the phenotypes that arise when microorganisms lack Mn(2+) are then discussed, with an emphasis on those phenotypes involving pathogenesis. The concluding section describes possible enzymatic roles for Mn(2+) that might help explain why Mn(2+) is necessary for virulence.
最近，两个研究领域的成果汇聚在一起，凸显了锰离子（Mn(2+)）在发病机制中的重要作用：一是认识到细菌Nramp同源物和LraI蛋白家族成员都是锰离子转运蛋白；二是它们的突变与多种细菌毒力降低有关。因此，锰离子似乎对细菌毒力至关重要。本综述描述了目前关于原核生物中锰离子转运的已知情况，以及原核生物锰离子转运是如何被调控的。接着讨论了微生物缺乏锰离子时出现的一些表型，重点是那些涉及发病机制的表型。结论部分描述了锰离子可能的酶促作用，这或许有助于解释为什么锰离子对毒力是必需的。
