TY - JOUR
T1 - Nutritional immunity beyond iron
T2 - a role for manganese and zinc
AU - Kehl-Fie, Thomas E.
AU - Skaar, Eric P.
N1 - Funding Information:
We sincerely apologize to our colleagues whose work we were unable to cite owing to space limitations. This publication was made possible by NIH grant #U54 AI057157 from the Southeastern Regional Center of Excellence for Emerging Infections and Biodefense , and NIAID grants AI069233 and AI073843 to EPS. TKF is supported by National Institutes of Health fellowship T32 HL094296-02. The manuscript's contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH.
PY - 2010/4
Y1 - 2010/4
N2 - Vertebrates sequester iron from invading pathogens, and conversely, pathogens express a variety of factors to steal iron from the host. Recent work has demonstrated that in addition to iron, vertebrates sequester zinc and manganese both intracellularly and extracellularly to protect against infection. Intracellularly, vertebrates utilize the ZIP/ZnT families of transporters to manipulate zinc levels, as well as Nramp1 to manipulate manganese levels. Extracellularly, the S100 protein calprotectin sequesters manganese and potentially zinc to inhibit microbial growth. To circumvent these defenses, bacteria possess high affinity transporters to import specific nutrient metals. Limiting the availability of zinc and manganese as a mechanism to defend against infection expands the spectrum of nutritional immunity and further establishes metal sequestration as a key defense against microbial invaders.
AB - Vertebrates sequester iron from invading pathogens, and conversely, pathogens express a variety of factors to steal iron from the host. Recent work has demonstrated that in addition to iron, vertebrates sequester zinc and manganese both intracellularly and extracellularly to protect against infection. Intracellularly, vertebrates utilize the ZIP/ZnT families of transporters to manipulate zinc levels, as well as Nramp1 to manipulate manganese levels. Extracellularly, the S100 protein calprotectin sequesters manganese and potentially zinc to inhibit microbial growth. To circumvent these defenses, bacteria possess high affinity transporters to import specific nutrient metals. Limiting the availability of zinc and manganese as a mechanism to defend against infection expands the spectrum of nutritional immunity and further establishes metal sequestration as a key defense against microbial invaders.
UR - http://www.scopus.com/inward/record.url?scp=77949885386&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77949885386&partnerID=8YFLogxK
U2 - 10.1016/j.cbpa.2009.11.008
DO - 10.1016/j.cbpa.2009.11.008
M3 - Review article
C2 - 20015678
AN - SCOPUS:77949885386
VL - 14
SP - 218
EP - 224
JO - Current Opinion in Chemical Biology
JF - Current Opinion in Chemical Biology
SN - 1367-5931
IS - 2
ER -