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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using 58Fe, 51Cr and cytological parameters, the authors have examined erythropoiesis in 44 polycythaemia vera patients diagnosed as such on the basis of the usual parameters (exept for determination of the erythropoietin level). In the patients divided into four types the following characteristica were observed. In type I, increased erythropoiesis is evident by accelerated plasma iron clearance, greater PIT and EIT as well as enhanced iron utilization and production indices. In type II, in addition to the former signs of increased erythropoiesis moderately shortened red cell life-span and hyposideraemia characteristic of splenic sequestration and resulting from bleeding and blood letting seem to be accompanied by microcytosis. There is a metaplastic erythropoiesis in type III, bone marrow activity decreases, but the increased erythropoiesis is indicated by several parameters already observed earlier. At the time the iron utilization indicative of effective erythropoiesis is decreased, thus ineffective erythropoiesis and considerably shortened red cell life-span are responsible for the enhanced iron turnover. This is also shown by the regression calculations. In type IV effective erythropoiesis was considerably decreased in the patients with severe anaemia. Sings which are indicative of metaplastic erythropoiesis are absent. In one of the patients the morphological changes characteristic of dyserythropoiesis were found. Although all our patients were given treatment. We believe that these alterations in the character of erythropoiesis are not likely to be the consequences of therapy.
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PMID:Changes in erythropoiesis during the course of polycythaemia vera. 6 14

Morphological parameters of the red cells were studied in 121 patients with typhoid-paratyphoid conditions. To obtain objective clinical data the authors studied the effect of LPS S. anatum on the intact red cells of healthy persons. The correlation of morphological disorders in the red cells of the patients and the controls revealed a significant role of intoxication in their origin. The research conducted revealed a relationship between the disorders in the erythrocyte membranes and the development of anemia in the patients.
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PMID:[Pathogenesis of anemia in abdominal typhus]. 150 35

Immunosenescence occurs with aging, which is seen in decline in response to mitogens PHA, ConA, decline in cell-mediated immunity, increase in anemia, and increase in autoimmune antibodies to erythrocytes and DNA. These studies compared FTS, TP5, TM4, and TF5 in C57BL/6NNia mice. Mice aged 4, 26, 52, 78 and 104 wk were treated with various hormones 5x/wk for 3 wk and monitored for hormonal effects on weight; hematocrit; peripheral blood, spleen, and thymic cell numbers; spleen and peripheral blood cell mitogen responses to PHA, ConA, LPS; IgM hemolysin autoantibody; and cell-mediated cytotoxicity to P815 allogenic cells. Hormone treatments altered mitogen responses, enhanced IgM hemolysin autoantibody production, and modulated cell-mediated immune responses. The effects were not consistent for every hormone. There was a tendency for enhancement in younger mice and suppression in older animals. Treatment with FTS showed the greatest changes in either enhancing or suppressing the different parameters measured. The hormonal effects appeared to be age specific in that certain activities were altered for certain age groups but not in others. Hormone treatment did not restore any immune parameters in old mice to the level of young animals. In general, the different hormones did not consistently produce the same effects in C57BL/6NNia mice of different age groups. Even though all animals received from National Institutes on Aging (NIA) animal models program were held under strictly controlled conditions, intrinsic variations between cohorts of different ages are difficult to control. Cohorts of aging animals tested at different times might be intrinsically different. This inherent variability in the cohorts could affect the range of activity, specificity and reproducibility of hormone effects in vivo. Most importantly, it should be emphasized that cross-sectional data identifies age differences rather than age changes. There is no assurance that age changes in any individual or in all subpopulations follow this pattern. In our studies only healthy animals were used. Old, sick, or tumor-bearing animals were culled out prior to being sent to us. Therefore, the 78- and 104-wk-old mice represent selected healthy cohorts. The age changes that take place can be answered only from repeated measurements made in the same individual over time.
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PMID:Survey of thymic hormone effects on physical and immunological parameters in C57BL/6NNia mice of different ages. 185 89

Eight daily intraperitoneal injections of endotoxin (LPS) induced hematologic abnormalities in mice like those previously observed with chronic inflammation, sterile abscess, and tumor bearing. By the ninth day, anemia, leukocytosis, hypocellularity of the bone marrow, and compensatory hemopoietic hyperplasia of the spleen had occurred. The suppressed hemopoietic recovery and impaired survival of mice with these abnormalities, after receiving an ordinarily sublethal dose of total body irradiation (600 cGy T.B.), confirmed their importance to the intact mouse and suggested that splenic hyperplasia was insufficient to compensate for a total body deficit of functional hemopoietic stem cells. Atrophy of hemopoietic tissue in the marrow with hyperplasia in the spleen implicated changes in the hemopoietic microenvironment to account for the different responses to endotoxin. Prostaglandin E2 (PGE2) serves as an important mediator of the inflammatory response and profoundly affects hemopoiesis. Previous studies had shown that low concentrations of PGE2 enhanced, and high concentrations suppressed erythropoiesis in vitro; therefore, we wondered whether stromal cells from the marrow's microenvironment produced more PGE2 in response to LPS than splenic stromal cells to explain the suppression of hemopoiesis in the marrow and its enhancement in the spleen. Indeed, synthesis of PGE2 in primary short-term cultures of adherent marrow stromal cells in response to LPS proved much greater than that observed in cultures of splenic stromal cells. Extending adherence times from 3 to 24 to 48 hours did not change the relationship. We believe that the results of our studies point to a role of PGE2 in the microenvironmental modulation of hemopoiesis in mice with activation of the inflammatory response.
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PMID:Differential elaboration of prostaglandin E2 by cells of the hemopoietic microenvironment in response to endotoxin. 329 86

In vitro monocyte-derived tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) production was assessed in iron deficient with anemia (IDA), iron deficient without anemia (ID) and control infants. The concentrations of released and cell-associated cytokines were measured before and after 3 months of iron supplementation in all groups (ferrous sulphate drops: 3 mg/Kg/day). No difference in released and cell-associated IL-1 beta was observed between either groups of infants. Lipopolysaccharide-stimulated blood mononuclear cells from IDA (n = 9) infants produced a significantly higher immunoreactive TNF-alpha concentration as compared to ID (n = 9) and normal subjects (n = 18) on admission (F = 6.72; p < 0.004). After iron therapy, the LPS stimulated TNF-alpha secretion by cells of IDA infants returned to the levels observed in the other groups. Since TNF-alpha plays a key role in iron metabolism, we speculate that increased TNF production in IDA infants could exacerbate the inhibition of erythroid proliferation present in these conditions. Further studies are needed to evaluate the effect of more severe anemia as well as to clarify the biological effect of increased TNF-alpha production in iron deficiency anemia and its consequences.
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PMID:Increased in vitro tumour necrosis factor-alpha production in iron deficiency anemia. 784 56

Decreased production of erythropoietin (Epo) as a result of reduced renal mass is considered the main factor underlying the anaemia that is invariably associated with chronic renal failure (CRF). Other mechanisms such as accumulation of inhibitors of Epo also contribute. In this study we show that supernatant from peripheral blood mononuclear cells (PBMC) cultured from patients with CRF inhibits Epo release by Hep G2 cells in vitro. Ten patients (5 male) with CRF (mean age 42 years, range 25-60) were studied. Five were approaching end-stage renal failure and five were maintained on haemodialysis (HD). Ten apparently healthy volunteers were used as controls. Full blood counts and serum Epo (RIA) levels were determined and adherent PBMC were cultured for 48 h with and without LPS. There was a significant rise in TNF-alpha and IL1-beta levels measured in monocyte supernatant (MS) from patients and controls after LPS stimulation (P < 0.05) and in IL-1 alpha levels in patients (P < 0.05). IL-1 beta levels were higher in patients compared to controls both before and after stimulation with LPS (P < 0.05). Hep G2 cells were cultured in 5% CO2 and 20% O2 and incubated with MS from patients and controls for 24 h. Hep G2 harvest fluids were then analysed for Epo levels, which were expressed as a function of total cell protein (mU/mg). Epo production was inhibited by MS from patients compared to controls both before and after stimulation with LPS (P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Peripheral blood mononuclear cells from patients with chronic renal failure release factors which suppress erythropoietin secretion in vitro. 797 Jan 19

IL-13, a recently identified Th2 cytokine, shares some, but not all, IL-4 functions, including inhibition of monocyte and macrophage activation, stimulation of human B cells, and induction of growth and differentiation of mouse bone marrow cells in vitro. We have now tested the in vivo effects of recombinant mouse IL-13 (rIL-13) from stably transfected, high expressing BW5147 thymoma cells. After purification by anion exchange chromatography, rIL-13 was administered in the peritoneal cavity of BALB/c mice via osmotic pump for 7 days. Spleens from the rIL-13-treated mice were significantly enlarged compared with control spleens due to increased cellularity. In particular, increased numbers of immature erythroblasts and megakaryocytes were observed in splenic sections after rIL-13 treatment. Spleen cells from rIL-13-treated mice showed greatly increased responsiveness in vitro to recombinant forms of mouse IL-3, mouse granulocyte-macrophage CSF, or human CSF-1 and, to a lesser extent, to mouse IL-4 or IL-13. Moreover, the rIL-13-treated mice also showed significant increases in CFU-E, CFU-C, and erythroid burst colonies in the spleen, further indicating the presence of increased numbers of hemopoietic precursors. Hematologic analyses indicated that rIL-13 treatment induced slight anemia and striking monocytosis. Finally, spleen cells from rIL-13-treated mice produced significantly more IL-6 upon LPS stimulation. Interestingly, the strong Th2 response induced by Nippostrongylus brasiliensis infection was also accompanied by an increase in hemopoietic precursor frequencies in the spleen. Collectively, these data indicate that exogenous rIL-13 induces extramedullary hemopoiesis in mice and suggest that endogenous IL-13 may contribute to replenishment of effector cells during strong Th2 responses.
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PMID:Continuous administration of Il-13 to mice induces extramedullary hemopoiesis and monocytosis. 861 37

Intravenous Fe is widely used to treat anemia in renal disease patients. However, concerns of potential Fe toxicity exist. To more fully define its spectrum, this study tested Fe's impact on systemic inflammation following either endotoxemia or the induction of direct tissue damage (glycerol-mediated rhabdomyolysis). The inflammatory response was gauged by tissue TNF-alpha message expression and plasma TNF-alpha levels. CD-1 mice received either intravenous Fe sucrose, -gluconate, or -dextran (FeS, FeG, or FeD, respectively; 2 mg), followed by either endotoxin (LPS) or glycerol injection 0-48 h later. Plasma TNF-alpha was assessed by ELISA 2-3 h after the LPS or glycerol challenge. TNF-alpha mRNA expression (RT-PCR) was measured in the kidney, heart, liver, lung, and spleen with Fe +/- LPS treatment. Finally, the relative impacts of intramuscular vs. intravenous Fe and of glutathione (GSH) on Fe/LPS- induced TNF-alpha generation were assessed. Each Fe preparation significantly enhanced LPS- or muscle injury-mediated TNF-alpha generation. This effect was observed for at least 48 h post-Fe injection, a time at which plasma iron levels were increased by levels insufficient to fully saturate transferrin. Fe did not independently increase plasma TNF-alpha or tissue mRNA. However, it potentiated postinjury-induced TNF-alpha mRNA increments and did so in an organ-specific fashion (kidney, heart, and lung; but not in liver or spleen). Intramuscular administration, but not GSH treatment, negated Fe's ability to synergize LPS-mediated TNF-alpha release. We conclude 1) intravenous Fe can enhance TNF-alpha generation during LPS- or glycerol-induced tissue damage; 2) increased TNF-alpha gene transcription in the kidney, heart, and lung may contribute to this result; and 3) intramuscular administration, but not GSH, might potentially mitigate some of Fe's systemic toxic effects.
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PMID:Parenteral iron compounds sensitize mice to injury-initiated TNF-alpha mRNA production and TNF-alpha release. 1549 44

Interleukin-10 (IL-10) is a well known anti-inflammatory cytokine. However, we previously showed that it could present pro-inflammatory properties on human monocytes in the absence of adherence. In the present study, using macroarray technology, we analyzed the effects of IL-10 and adherence on the expression of 1050 genes in human monocytes cultured for 3 hours on plastic or Teflon(R) (to avoid adherence). Adherence alone induced specifically the expression of 12 genes and repressed that of 25 genes. In adherent monocytes, IL-10 induced the expression of 21 genes and repressed that of 50 genes. In non-adherent monocytes, IL-10 induced the expression of 45 genes and repressed that of 67. Only 3 common genes were induced while 35 common genes were repressed by IL-10 in the two culture conditions. Interestingly, we showed that IL-10 modulated conversely on Teflon(R) and plastic the expression of 16 genes, of which SOCS molecules, coproporphyrinogen oxidase, matrix metalloproteinases and complement receptor-1 (CD35). This study demonstrates that adherence has profound modulatory effects on the properties and the signaling induced by IL-10. The discovery that IL-10 can inhibit the production of coproporphyrinogen oxidase (an enzyme involved in the synthesis of heme) may shed some lights on the mechanisms of anaemia induced by IL-10. Furthermore, the inhibition of the expression of SOCS1 by IL-10 in the absence of adherence, may explain its priming effects on a subsequent LPS stimulation that we previously described.
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PMID:Adherence modifies the regulation of gene expression induced by interleukin-10. 1557 72

Patients with the genomic instability syndrome Fanconi anemia (FA) commonly develop progressive bone marrow (BM) failure and have a high risk of cancer. Certain manifestations of the disease suggest that the FA immune system is dysfunctional and may contribute to the pathogenesis of both BM failure and malignancies. In this study, we have investigated inflammation and innate immunity in FA hemopoietic cells using mice deficient in Fanconi complementation group C gene (Fancc). We demonstrate that Fancc-deficient mice exhibit enhanced inflammatory response and are hypersensitive to LPS-induced septic shock as a result of hemopoietic suppression. This exacerbated inflammatory phenotype is intrinsic to the hemopoietic system and can be corrected by the re-expression of a wild-type FANCC gene, suggesting a potential role of the FANCC protein in innate immunity. LPS-mediated hemopoietic suppression requires two major inflammatory agents, TNF-alpha and reactive oxygen species. In addition, LPS-induced excessive accumulation of reactive oxygen species in Fancc(-/-) BM cells overactivates the stress kinase p38 and requires prolonged activation of the JNK. Our data implicate a role of inflammation in pathogenesis of FA and BM failure diseases in general.
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PMID:Inflammatory reactive oxygen species-mediated hemopoietic suppression in Fancc-deficient mice. 1740 12


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