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- W2613230166 startingPage "211" @default.
- W2613230166 abstract "Transition metals are essential nutrients for all organisms and important players in the host-microbe interaction. During bacterial infection, a tug-of-war between the host and microbe for nutrient metals occurs: the host innate immune system responds to the pathogen by reducing metal availability and the pathogen tries to outmaneuver this response. The outcome of this competition, which involves metal-sequestering host-defense proteins and microbial metal acquisition machinery, is an important determinant for whether infection occurs. One strategy bacterial pathogens employ to overcome metal restriction involves hijacking abundant host metalloproteins. The obligate human pathogens Neisseria meningitidis and N. gonorrhoeae express TonB-dependent transport systems that capture human metalloproteins, extract the bound metal ions, and deliver these nutrients into the bacterial cell. This review highlights structural and mechanistic investigations that provide insights into how Neisseria acquire iron from the Fe(III)-transport protein transferrin (TF), the Fe(III)-chelating host-defense protein lactoferrin (LF), and the oxygen-transport protein hemoglobin (Hb), and obtain zinc from the metal-sequestering antimicrobial protein calprotectin (CP)." @default.
- W2613230166 created "2017-05-19" @default.
- W2613230166 creator A5064331450 @default.
- W2613230166 creator A5066305106 @default.
- W2613230166 creator A5085950326 @default.
- W2613230166 date "2017-05-09" @default.
- W2613230166 modified "2023-09-26" @default.
- W2613230166 title "Transition metals at the host–pathogen interface: how<i>Neisseria</i>exploit human metalloproteins for acquiring iron and zinc" @default.
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