TY - JOUR
T1 - Iron deficiency and neutrophil function
T2 - Different rates of correction of the depressions in oxidative burst and myeloperoxidase activity after iron treatment
AU - Murakawa, H.
AU - Bland, C. E.
AU - Willis, W. T.
AU - Dallman, P. R.
PY - 1987
Y1 - 1987
N2 - The polymorphonuclear granulocyte (PMN) kills ingested bacteria by mechanisms that include myeloperoxidase (MPO) and a sudden increase in oxygen consumption (the oxidative burst), both of which are iron dependent. The magnitude of the oxidative burst and activity of MPO were determined in PMNs during the progression of iron deficiency (ID) and following its treatment in rats. As ID developed, the oxidative burst after zymosan activation was less depressed than the activity of MPO. There was no change in the oxidative burst after activation with phorbol myristate acetate (PMA) or in the generation of superoxide (O2-) by NADPH oxidase-containing particles from PMNs. Following iron treatment, impairment of the oxidative burst after zymosan activation was corrected after 1 day. In contrast, the deficit in MPO activity was not corrected until 7 days after initiation of iron treatment. The pattern of recovery in MPO activity after iron treatment corresponded to the prolonged period of maturation of the PMN primary granule since the formation of primary granules, which contain MPO, takes place only in the early, mitotic stages of maturation. The tendency of the PMN to maintain the oxidative burst allows the cell to preserve its capacity for bacterial killing during the progression of iron deficiency.
AB - The polymorphonuclear granulocyte (PMN) kills ingested bacteria by mechanisms that include myeloperoxidase (MPO) and a sudden increase in oxygen consumption (the oxidative burst), both of which are iron dependent. The magnitude of the oxidative burst and activity of MPO were determined in PMNs during the progression of iron deficiency (ID) and following its treatment in rats. As ID developed, the oxidative burst after zymosan activation was less depressed than the activity of MPO. There was no change in the oxidative burst after activation with phorbol myristate acetate (PMA) or in the generation of superoxide (O2-) by NADPH oxidase-containing particles from PMNs. Following iron treatment, impairment of the oxidative burst after zymosan activation was corrected after 1 day. In contrast, the deficit in MPO activity was not corrected until 7 days after initiation of iron treatment. The pattern of recovery in MPO activity after iron treatment corresponded to the prolonged period of maturation of the PMN primary granule since the formation of primary granules, which contain MPO, takes place only in the early, mitotic stages of maturation. The tendency of the PMN to maintain the oxidative burst allows the cell to preserve its capacity for bacterial killing during the progression of iron deficiency.
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U2 - 10.1182/blood.v69.5.1464.1464
DO - 10.1182/blood.v69.5.1464.1464
M3 - Article
C2 - 3032307
AN - SCOPUS:0023226442
SN - 0006-4971
VL - 69
SP - 1464
EP - 1468
JO - Blood
JF - Blood
IS - 5
ER -