Mouse
transferrin was used to specifically label the plasma
transferrin iron pool for studies of
iron kinetics in normal mice and infected mice during the hypoferremic phase of experimental
meningococcal infection. The plasma
transferrin iron pool of normal mice was found to be very dynamic, with a half-life of
iron in the pool of 0.7 h.
Iron left the plasma pool, entered the bone marrow, and was released into the blood in erythrocytes.
Iron from the
transferrin pool also entered the liver and spleen and was presumably in the reticuloendothelial system components of these organs. Most of the
iron that had been supplied as
transferrin iron was found in erythrocytes by 48 h after injection. Studies with mice infected with Neisseria meningitidis strain M1011 revealed similar kinetics for
transferrin iron. There was no redistribution of
iron within the various
iron pools as a result of
infection.
Iron turnover in the plasma
transferrin pool during the hypoferremic phase was similar to control rates, and
iron leaving the pool entered its normal erythroid compartments. The lack of accelerated turnover of plasma
iron and the finding that plasma
iron was not rerouted to storage compartments during the hypoferremic phase provided good evidence that
lactoferrin and leukocytic endogenous mediator were not directly involved in redirecting
transferrin iron. Our evidence has implicated an impaired return of reticuloendothelial system-processed
iron to the
transferrin pool during the hypoferremic response. This appears to be a logical point in the erythroid
iron cycle for host-mediated
iron sequestration, as the reticuloendothelial system is involved in
iron storage and may regulate
iron levels in the plasma
transferrin pool under normal conditions.