TY - JOUR
T1 - Iron acquisition from Pseudomonas aeruginosa siderophores by human phagocytes
T2 - An additional mechanism of host defense through iron sequestration?
AU - Britigan, Bradley E.
AU - Rasmussen, George T.
AU - Olakanmi, Oyebode
AU - Cox, Charles D.
PY - 2000
Y1 - 2000
N2 - Chelation of iron to iron-binding proteins is a strategy of host defense. Some pathogens counter this via the secretion of low-molecular- weight iron-chelating agents (siderophores). Human phagocytes possess a high- capacity mechanism for iron acquisition from low-molecular-weight iron chelates. Efficient acquisition and sequestration of iron bound to bacterial siderophores by host phagocytes could provide a secondary mechanism to limit microbial access to iron. In the present work we report that human neutrophils, macrophages, and myeloid cell lines can acquire iron from the two Pseudomonas aeruginosa siderophores. Analogous to iron acquisition from other low-molecular-weight chelates, iron acquisition from the siderophores is ATP independent, induced by multivalent cationic metals, and unaffected by inhibitors of endocytosis and pinocytosis. In vivo, this process could serve as an additional mechanism of host defense to limit iron availability to invading siderophore-producing microbes.
AB - Chelation of iron to iron-binding proteins is a strategy of host defense. Some pathogens counter this via the secretion of low-molecular- weight iron-chelating agents (siderophores). Human phagocytes possess a high- capacity mechanism for iron acquisition from low-molecular-weight iron chelates. Efficient acquisition and sequestration of iron bound to bacterial siderophores by host phagocytes could provide a secondary mechanism to limit microbial access to iron. In the present work we report that human neutrophils, macrophages, and myeloid cell lines can acquire iron from the two Pseudomonas aeruginosa siderophores. Analogous to iron acquisition from other low-molecular-weight chelates, iron acquisition from the siderophores is ATP independent, induced by multivalent cationic metals, and unaffected by inhibitors of endocytosis and pinocytosis. In vivo, this process could serve as an additional mechanism of host defense to limit iron availability to invading siderophore-producing microbes.
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U2 - 10.1128/IAI.68.3.1271-1275.2000
DO - 10.1128/IAI.68.3.1271-1275.2000
M3 - Article
C2 - 10678937
AN - SCOPUS:0033969663
SN - 0019-9567
VL - 68
SP - 1271
EP - 1275
JO - Infection and immunity
JF - Infection and immunity
IS - 3
ER -