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X Alvarez-Hernández

Publications and source records attributed to X Alvarez-Hernández.

9 recordsLinked to original sources
PubMed1989

Induction of hypoferremia and modulation of macrophage iron metabolism by tumor necrosis factor.

The effects of recombinant tumor necrosis factor (TNF), tumor necrosis serum (TNS), recombinant interleukin 1 (IL-1), and prostaglandin E2 on serum iron parameters and iron handling by macrophages in mice have been investigated. Recombinant TNF caused a significant decrease in serum iron levels after 6 hours, but none of the mediators caused significant changes in total iron binding capacity at this time, although TNS caused a significant increase in total iron binding capacity after 24 hours. Peritoneal macrophages taken from mice 6 hours after inoculation of the mediators were pulsed with 59Fe, 125I-transferrin-antitransferrin immune complexes, and subsequent degradation of the complexes and release of iron were investigated. Both recombinant TNF and TNS caused significant increases in uptake and degradation of the complexes, but with recombinant TNF this was not accompanied by a corresponding increase in iron release. IL-1 and prostaglandin E2 also caused increased degradation of the immune complexes, but uptake of the complexes and iron release were unaffected. When peritoneal macrophages from normal mice were treated with the mediators in vitro and then pulsed with labeled immune complexes, recombinant TNF caused a significant decrease in iron release, but none of the other mediators had any effect. None of the mediators affected uptake or degradation of the immune complexes. These results suggest that TNF, rather than IL-1, mediates the hypoferremia of inflammatory disease and that alterations in the ability of macrophages to handle iron may be responsible.

Animals↗
PubMed1988

Uptake and handling of iron from transferrin, lactoferrin and immune complexes by a macrophage cell line.

The murine macrophage-like cell line P388D1 has been used as a model to investigate whether iron acquired simultaneously from different sources (transferrin, lactoferrin, and ovotransferrin-anti-ovotransferrin immune complexes) is handled in the same way. P388D1 cells bound both lactoferrin and transferrin, but over a 6 h incubation period only the latter actually donated iron to the cells. When the cells were incubated with [55Fe]transferrin and [59Fe]ovotransferrin-anti-ovotransferrin immune complexes iron was acquired from both sources. However, there was a difference in the intracellular distribution of the two isotopes, proportionally more 55Fe entering haem compounds and less entering ferritin. When the cells were precultured in a low-iron serum-free medium almost no transferrin-iron was incorporated into ferritin, whereas the proportion of immune complex-derived iron incorporated into ferritin was unchanged. Lactoferrin enhanced the rate of cellular proliferation, as measured by [3H]thymidine incorporation, despite its inability to donate iron to the cells, suggesting a stimulatory effect independent of iron donation. In contrast immune complexes inhibited cell proliferation. These findings indicate that iron acquired from transferrin and iron acquired by scavenging mechanisms are handled differently, and suggest that more than one intracellular iron transit pool may exist.

Antigen-Antibody Complex↗
PubMed1986

The relationship between iron release, ferritin synthesis and intracellular iron distribution in mouse peritoneal macrophages. Evidence for a reduced level of metabolically available iron in elicited macrophages.

The rate of iron release from thioglycollate-elicited mouse peritoneal macrophages pulsed with 59Fe-labelled transferrin-antitransferrin immune complexes was lower than that from resident or Corynebacterium parvum-activated macrophages. Anaerobic conditions increased the rate of iron release by thioglycollate-elicited macrophages but had no effect on resident or C. parvum-activated macrophages. Thioglycollate-elicited macrophages also contained less ferritin and were deficient in their ability to synthesis ferritin. Incubation of these cells in medium containing 100 microM iron caused some increase in ferritin synthesis, but the response to iron was much less pronounced than that by resident or C. parvum-activated macrophages. In the thioglycollate-elicited macrophages, relatively less iron was incorporated into ferritin, and more into other soluble macromolecules and insoluble haemosiderin-like compounds than in the other types of macrophages. It is proposed that thioglycollate-elicited macrophages tend to divert iron to a relatively inert intracellular pool, and that this could account for their reduced ability to release iron. Such a mechanism might help to explain the reduced release of iron by liver and spleen macrophages occurring during inflammation.

Anaerobiosis↗
PubMed1984

Ferritin in normal human peripheral blood T-lymphocyte subpopulations.

Six peripheral blood lymphoid fractions (total lymphocytes, non-T, T, Tar (autologous rosette-forming T cells/precursor), T mu (helper), and T gamma (suppressor) lymphocytes) isolated through rosetting procedures were examined for the presence of ferritin by a direct immunofluorescence technique. Although ferritin was present in all lymphoid fractions studied, a significantly higher proportion of ferritin-containing cells were detected in the T-cell fraction than in the non-T-cell fraction, (mean +/- SD = 7.9 +/- 1.6% and 5.0 +/- 1.2%, respectively). T mu- and T gamma-cell fractions showed a twofold increase in the number of ferritin-positive cells (14.1 +/- 1.4% and 15.4 +/- 2.6%, respectively), as compared with Tar (7.0 +/- 0.9%)-and total lymphocyte (6.9 +/- 1.3%)-cell fractions. These results indicate that ferritin is preferentially distributed in T mu and T gamma lymphocytes and may constitute the basis for explaining some of the roles exercised by these cells in the control of other biological systems.

Cell Separation↗
PubMedDate not supplied

[Usefulness of certain hematologic parameters in the diagnosis of iron deficiency anemia in children and women].

The sensitivity and nonspecificity of parameters for the detection of iron deficiency: mean corpuscular volume (MCV); mean corpuscular hemoglobin (MCH); serum iron (SI); total iron binding capacity (TIBC); transferrin saturation (TS); free erythrocyte protoporphyrin (Epp) and serum ferritin (SF) were studied in 78 children from 0.2-3.9 years old and in 165 mothers. In children, MCH and TS were the parameters that showed the highest sensitivity and lowest nonspecificity: 97% of the anemic and non-anemic children were identified as iron deficient by MCH less than 25 pg and/or TS less than 17.5% and 0 and 6% of the children without iron deficiency showed MCH and TS below these values. MCH, SF and TS in the group of mothers were the tests with the highest sensitivity (97%, 88% and 79% respectively), and the nonspecificity of these parameters were 2.2%, 30% and 0.7% respectively. MCH seems to be a sensible and specific screening test for detecting possible cases of iron deficiency in both maternal and infant populations. The best tests to establish the deficiency appear to be TS of Epp tests in children, and TS plus SF in mothers.

Adult↗