Transition Metals at the Host–pathogen Interface: How Neisseria Exploit Human Metalloproteins for Acquiring Iron and Zinc
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nihms867923.pdf
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1.03 MB
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Author(s)
Neumann, Wilma
Hadley, Rose Currier
Nolan, Elizabeth Marie
Date Issued
May 2017
Journal
Essays In Biochemistry
Publisher
Portland Press
Citation
Neumann, Wilma et al. “Transition Metals at the Host–pathogen Interface: How Neisseria Exploit Human Metalloproteins for Acquiring Iron and Zinc.” Essays In Biochemistry 61, 2 (May 2017): 211–223 © 2017 The Author(s)
Version
Author's final manuscript
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).
MIT Department
Massachusetts Institute of Technology. Department of Chemistry
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Creative Commons Attribution-Noncommercial-Share Alike
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DOI of Published Version
https://doi.org/10.1042/EBC20160084
