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Tapani Ruutu - One of the best experts on this subject based on the ideXlab platform.
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Colony Formation by megakaryocyte progenitors in myelodysplatic syndromes.
European Journal of Haematology, 2009Co-Authors: Eeva Juvonen, Seija Partanen, Sakari Knuutila, Tapani RuutuAbstract:In vitro megakaryocytic Colony Formation by progenitors from the bone marrow was studied in 40 myelodysplastic syndrome patients. Megakaryocytic colonies were decreased in number or absent in 30 patients; only 10 showed normal Colony growth. The growth correlated to some extent with the FAB-class. Patients with normal Colony Formation had either RA or RARS, but also in these two FAB-types half of the patients showed reduced megakaryocytic Colony Formation. Only 1 out of 15 patients with RAEB or RAEBt had normal megakaryocyte growth. The patients with CMML did not show any megakaryocytic colonies. The growth of erythroid colonies was normal in 3 patients and reduced or absent in the others. All 3 with normal erythroid Colony Formation also showed normal megakaryocyte growth, and all patients with normal megakaryocyte Colony Formation also had normal granulocyte-macrophage Colony growth. Granulocyte-macrophage Colony and cluster Formation was normal in 17 patients. Defective Formation of megakaryocytic, erythroid, and granulocyte-macrophage colonies was seen in 22 patients, compatible with a defect in a pluripotent stem cell. Megakaryocytic Colony Formation had no obvious correlation with any specific chromosome abnormality, and the distribution of the growth patterns was almost similar in patients with a normal and those with an abnormal karyotype.
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Erythroid and granulocyte-macrophage Colony Formation in myelodysplastic syndromes
Scandinavian Journal of Haematology, 2009Co-Authors: Tapani Ruutu, Seija Partanen, R. Lintula, Lasse Teerenhovi, Sakari KnuutilaAbstract:Colony Formation by haematopoietic progenitors from the bone marrow was studied in 44 patients with a myelodysplastic syndrome. Erythroid progenitors BFU-E and CFU-E were cultured in methyl cellulose, and granulocyte-macrophage precursors CFU-GM in agar. 3 of 32 patients showed normal numbers of BFU-E colonies; in all the other cases the number of these colonies was below the normal range. CFU-E Colony Formation was subnormal in all cases. 23 of 44 patients grew normal numbers of colonies and clusters in CFU-GM cultures. These patients had refractory anaemia with ring sideroblasts (FAB-classification) or 5q-karyotype anomaly in the marrow. Patients lacking both of these findings exhibited reduced Colony Formation or excessive growth of colonies and/or clusters, with few exceptions. In conclusion, we found that erythroid Colony Formation was defective in all cases. Normal granulocyte-macrophage Colony Formation was associated with refractory anaemia with ring sideroblasts or the presence of 5q- karyotype anomaly.
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Spontaneous erythroid Colony Formation in the differential diagnosis of erythrocytosis.
European Journal of Haematology, 2009Co-Authors: S. Partanen, Eeva Juvonen, E. Ikkala, Tapani RuutuAbstract:Erythroid Colony Formation in vitro was studied in 80 patients with erythrocytosis. 43 of the patients had polycythaemia vera (PV), 18 patients had secondary erythrocytosis, 6 had normal red cell mass, and 13 patients were regarded as unclassified. Spontaneous erythroid Colony Formation, in the absence of exogenous erythropoietin in the cultures, was discovered in all patients with PV, whereas no patient with secondary erythrocytosis or with normal red cell mass showed this phenomenon. 8 of the 13 patients with unclassified erythrocytosis spontaneously formed erythroid colonies. 7 patient with unclassified erythrocytosis have been followed for 5 yr. 3 of the 4 patients with spontaneous Colony growth but none of the 3 without it can now be classified as PV. Thus, spontaneous erythroid Colony Formation indicates PV even in early and atypical cases. Therefore, the culture of erythroid progenitors is very useful in the differential diagnosis of problematic cases with erythrocytosis.
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Megakaryocyte Colony Formation by bone marrow progenitors in myelodysplasia syndromes
British Journal of Haematology, 2008Co-Authors: Eeva Juvonen, Seija Partanen, Sakari Knuutila, Tapani RuutuAbstract:Summary. Megakaryocytic Colony Formation by precursor cells from the bone marrow was investigated in 10 patients with a myelodysplastic syndrome. All but one exhibited abnormal Colony Formation: four showed no Colony Formation at all, while a decreased number of colonies was noticed in five. All of the patients showed defective Colony Formation by erythroid progenitors, but only four showed clearly abnormal granulocyte-macrophage Colony Formation. The defect in megakaryocytic progenitors seems to be more akin to the defects occurring in erythroid progenitors than to the defects seen in the granulocyte-macrophage lineage.
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Defective in-vitro Colony Formation of haematopoietic progenitors in patients with cartilage-hair hypoplasia and history of anaemia.
European Journal of Pediatrics, 1994Co-Authors: Eeva Juvonen, Tapani Ruutu, Outi Mäkitie, Anne Mäkipernaa, Ilkka Kaitila, Jukka RajantieAbstract:Cartilage-hair hypoplasia (CHH) is a metaphyseal chondrodysplasia with short-limbed short stature. The CHH gene has been recently mapped to chromosome 9, and a generalized defect in cellular proliferation has been suggested. Immunological and haematological abnormalities are common findings in CHH. In the present study erythroid, megakaryocyte, and granulocyte-macrophage Colony Formation in vitro by progenitors from bone marrow and blood was investigated in eight patients with CHH. All patients showed decreased erythroid and megakaryocyte Colony Formation. Only one patient had a normal granulocyte-macrophage growth, while the others showed decreased numbers of colonies. The defect in Colony Formation did not correlate with the haemoglobin concentration, platelet count or neutrophil count. The impaired growth was not caused by a decreased number of progenitors as shown by erythroid cultures. The erythroid progenitors were incapable of Colony Formation in culture conditions sufficient for Colony Formation by normal progenitors. In a more effectively stimulated culture assay the number of erythroid progenitors was normal or increased.
Eeva Juvonen - One of the best experts on this subject based on the ideXlab platform.
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Colony Formation by megakaryocyte progenitors in myelodysplatic syndromes.
European Journal of Haematology, 2009Co-Authors: Eeva Juvonen, Seija Partanen, Sakari Knuutila, Tapani RuutuAbstract:In vitro megakaryocytic Colony Formation by progenitors from the bone marrow was studied in 40 myelodysplastic syndrome patients. Megakaryocytic colonies were decreased in number or absent in 30 patients; only 10 showed normal Colony growth. The growth correlated to some extent with the FAB-class. Patients with normal Colony Formation had either RA or RARS, but also in these two FAB-types half of the patients showed reduced megakaryocytic Colony Formation. Only 1 out of 15 patients with RAEB or RAEBt had normal megakaryocyte growth. The patients with CMML did not show any megakaryocytic colonies. The growth of erythroid colonies was normal in 3 patients and reduced or absent in the others. All 3 with normal erythroid Colony Formation also showed normal megakaryocyte growth, and all patients with normal megakaryocyte Colony Formation also had normal granulocyte-macrophage Colony growth. Granulocyte-macrophage Colony and cluster Formation was normal in 17 patients. Defective Formation of megakaryocytic, erythroid, and granulocyte-macrophage colonies was seen in 22 patients, compatible with a defect in a pluripotent stem cell. Megakaryocytic Colony Formation had no obvious correlation with any specific chromosome abnormality, and the distribution of the growth patterns was almost similar in patients with a normal and those with an abnormal karyotype.
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Spontaneous erythroid Colony Formation in the differential diagnosis of erythrocytosis.
European Journal of Haematology, 2009Co-Authors: S. Partanen, Eeva Juvonen, E. Ikkala, Tapani RuutuAbstract:Erythroid Colony Formation in vitro was studied in 80 patients with erythrocytosis. 43 of the patients had polycythaemia vera (PV), 18 patients had secondary erythrocytosis, 6 had normal red cell mass, and 13 patients were regarded as unclassified. Spontaneous erythroid Colony Formation, in the absence of exogenous erythropoietin in the cultures, was discovered in all patients with PV, whereas no patient with secondary erythrocytosis or with normal red cell mass showed this phenomenon. 8 of the 13 patients with unclassified erythrocytosis spontaneously formed erythroid colonies. 7 patient with unclassified erythrocytosis have been followed for 5 yr. 3 of the 4 patients with spontaneous Colony growth but none of the 3 without it can now be classified as PV. Thus, spontaneous erythroid Colony Formation indicates PV even in early and atypical cases. Therefore, the culture of erythroid progenitors is very useful in the differential diagnosis of problematic cases with erythrocytosis.
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Megakaryocyte Colony Formation by bone marrow progenitors in myelodysplasia syndromes
British Journal of Haematology, 2008Co-Authors: Eeva Juvonen, Seija Partanen, Sakari Knuutila, Tapani RuutuAbstract:Summary. Megakaryocytic Colony Formation by precursor cells from the bone marrow was investigated in 10 patients with a myelodysplastic syndrome. All but one exhibited abnormal Colony Formation: four showed no Colony Formation at all, while a decreased number of colonies was noticed in five. All of the patients showed defective Colony Formation by erythroid progenitors, but only four showed clearly abnormal granulocyte-macrophage Colony Formation. The defect in megakaryocytic progenitors seems to be more akin to the defects occurring in erythroid progenitors than to the defects seen in the granulocyte-macrophage lineage.
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Megakaryocyte Colony Formation in chronic myeloid leukemia and myelofibrosis.
Leukemia Research, 2004Co-Authors: Eeva JuvonenAbstract:Colony Formation by megakaryocytic progenitors from the blood or bone marrow was studied in 22 patients with chronic myeloid leukemia (CML) and in 17 patients with idiopathic myelofibrosis (MF). Thirteen of the 22 CML patients showed megakaryocytic Colony Formation, when PHA-LCM and plasma of a patient with aplastic anemia were used as a source of Colony stimulating activity. Twelve of these 13 patients also showed spontaneous megakaryocytic growth, i.e. Colony Formation when PHA-LCM was omitted and normal plasma was used instead of aplastic plasma. All the untreated CML patients exhibited both stimulated and spontaneous growth. Each patient without any megakaryocytic Colony Formation had recently received cytotoxic treatment. Thirteen of the 17 patients with MF grew megakaryocytic colonies and ten of these 13 patients also showed spontaneous megakaryocytic growth. The Colony numbers were roughly similar in the stimulated and non-stimulated cultures. The present study shows that spontaneous megakaryocytic Colony Formation, previously shown to be common in PV and ET, is also seen in many patients with CML and MF.
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Defective in-vitro Colony Formation of haematopoietic progenitors in patients with cartilage-hair hypoplasia and history of anaemia.
European Journal of Pediatrics, 1994Co-Authors: Eeva Juvonen, Tapani Ruutu, Outi Mäkitie, Anne Mäkipernaa, Ilkka Kaitila, Jukka RajantieAbstract:Cartilage-hair hypoplasia (CHH) is a metaphyseal chondrodysplasia with short-limbed short stature. The CHH gene has been recently mapped to chromosome 9, and a generalized defect in cellular proliferation has been suggested. Immunological and haematological abnormalities are common findings in CHH. In the present study erythroid, megakaryocyte, and granulocyte-macrophage Colony Formation in vitro by progenitors from bone marrow and blood was investigated in eight patients with CHH. All patients showed decreased erythroid and megakaryocyte Colony Formation. Only one patient had a normal granulocyte-macrophage growth, while the others showed decreased numbers of colonies. The defect in Colony Formation did not correlate with the haemoglobin concentration, platelet count or neutrophil count. The impaired growth was not caused by a decreased number of progenitors as shown by erythroid cultures. The erythroid progenitors were incapable of Colony Formation in culture conditions sufficient for Colony Formation by normal progenitors. In a more effectively stimulated culture assay the number of erythroid progenitors was normal or increased.
Seija Partanen - One of the best experts on this subject based on the ideXlab platform.
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Colony Formation by megakaryocyte progenitors in myelodysplatic syndromes.
European Journal of Haematology, 2009Co-Authors: Eeva Juvonen, Seija Partanen, Sakari Knuutila, Tapani RuutuAbstract:In vitro megakaryocytic Colony Formation by progenitors from the bone marrow was studied in 40 myelodysplastic syndrome patients. Megakaryocytic colonies were decreased in number or absent in 30 patients; only 10 showed normal Colony growth. The growth correlated to some extent with the FAB-class. Patients with normal Colony Formation had either RA or RARS, but also in these two FAB-types half of the patients showed reduced megakaryocytic Colony Formation. Only 1 out of 15 patients with RAEB or RAEBt had normal megakaryocyte growth. The patients with CMML did not show any megakaryocytic colonies. The growth of erythroid colonies was normal in 3 patients and reduced or absent in the others. All 3 with normal erythroid Colony Formation also showed normal megakaryocyte growth, and all patients with normal megakaryocyte Colony Formation also had normal granulocyte-macrophage Colony growth. Granulocyte-macrophage Colony and cluster Formation was normal in 17 patients. Defective Formation of megakaryocytic, erythroid, and granulocyte-macrophage colonies was seen in 22 patients, compatible with a defect in a pluripotent stem cell. Megakaryocytic Colony Formation had no obvious correlation with any specific chromosome abnormality, and the distribution of the growth patterns was almost similar in patients with a normal and those with an abnormal karyotype.
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Erythroid and granulocyte-macrophage Colony Formation in myelodysplastic syndromes
Scandinavian Journal of Haematology, 2009Co-Authors: Tapani Ruutu, Seija Partanen, R. Lintula, Lasse Teerenhovi, Sakari KnuutilaAbstract:Colony Formation by haematopoietic progenitors from the bone marrow was studied in 44 patients with a myelodysplastic syndrome. Erythroid progenitors BFU-E and CFU-E were cultured in methyl cellulose, and granulocyte-macrophage precursors CFU-GM in agar. 3 of 32 patients showed normal numbers of BFU-E colonies; in all the other cases the number of these colonies was below the normal range. CFU-E Colony Formation was subnormal in all cases. 23 of 44 patients grew normal numbers of colonies and clusters in CFU-GM cultures. These patients had refractory anaemia with ring sideroblasts (FAB-classification) or 5q-karyotype anomaly in the marrow. Patients lacking both of these findings exhibited reduced Colony Formation or excessive growth of colonies and/or clusters, with few exceptions. In conclusion, we found that erythroid Colony Formation was defective in all cases. Normal granulocyte-macrophage Colony Formation was associated with refractory anaemia with ring sideroblasts or the presence of 5q- karyotype anomaly.
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Spontaneous erythroid Colony Formation in erythrocytosis.
Acta Medica Scandinavica, 2009Co-Authors: Seija PartanenAbstract:. Erythroid Colony Formation from the bone marrow and blood of 30 patients with erythrocytosis has been studied. Seventeen patients formed spontaneous erythroid colonies. They included patients with polycythaemia vera (PV) and 4 patients who did not quite fulfil the Polycythemia Vera Study Group criteria for PV, but had suggestive evidence of a myeloproliferative disorder. Thirteen patients did not form spontaneous colonies. They included patients with secondary polycythaemia, patients with normal total red cell volume and patients with absolute pure erythrocytosis of unknown origin. All patients with PV, and none with secondary polycythaemias, had spontaneous erythroid Colony Formation. Three of 4 untreated and 2 of 9 treated PV patients had increased number of CFU-E colonies in bone marrow. From these results it can be concluded that erythroid progenitor cell culture is a useful differential diagnostic method in erythrocytosis patients who cannot be classified clinically under PV or secondary polycythaemias.
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Megakaryocyte Colony Formation by bone marrow progenitors in myelodysplasia syndromes
British Journal of Haematology, 2008Co-Authors: Eeva Juvonen, Seija Partanen, Sakari Knuutila, Tapani RuutuAbstract:Summary. Megakaryocytic Colony Formation by precursor cells from the bone marrow was investigated in 10 patients with a myelodysplastic syndrome. All but one exhibited abnormal Colony Formation: four showed no Colony Formation at all, while a decreased number of colonies was noticed in five. All of the patients showed defective Colony Formation by erythroid progenitors, but only four showed clearly abnormal granulocyte-macrophage Colony Formation. The defect in megakaryocytic progenitors seems to be more akin to the defects occurring in erythroid progenitors than to the defects seen in the granulocyte-macrophage lineage.
Robert T. Means - One of the best experts on this subject based on the ideXlab platform.
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Hepcidin Inhibits Erythroid Colony Formation In Vitro at Decreased Erythropoietin Concentrations.
Blood, 2005Co-Authors: Robert T. Means, Gail Dallalio, Erin LawAbstract:The anemia of chronic disease (ACD) results from three major processes: slightly shortened red cell survival, impaired reticuloendothelial system iron mobilization, and impaired erythropoiesis. Hepcidin is an acute phase protein with specific iron regulatory properties, which, along with the anemia seen with increased hepcidin expression, have led many to consider it the major mediator of ACD. However, if hepcidin is the major factor responsible for ACD, then it should also contribute to the impaired erythropoiesis observed in this syndrome. In this study, the effects of hepcidin on erythroid Colony Formation in vitro are examined. At the standard recombinant human erythropoietin (rhEPO) concentration used for erythroid Colony-forming unit (CFU-E) assays in vitro (1 U/mL), hepcidin had no significant effects on Colony Formation. However, ACD is a syndrome associated with relative reductions in EPO concentration. The effects of hepcidin 100 ng/mL on CFU-E Colony Formation were evaluated at lower rhEPO concentrations (0.1 _ 0.5 U/mL). Colony Formation was significantly decreased in the presence of hepcidin. The regulatory pathways controlling apoptosis and proliferation of HCD57 erythroleukemia cells replicate those observed in primary human erythroid progenitors. This cell line was studied in order to more fully define the effects of hepcidin on erythropoiesis. HCD57 cells were incubated in Iscove’s modified Dulbecco’s medium with 10% fetal calf serum with 0.3 U/mL rhEPO at 37°C for 24 hrs, with or without hepcidin 100 ng/mL. No difference in cell proliferation was seen. Apoptosis in HCD57 cells is regulated by the Bad/Bcl-x L pathway. Total Bad and Bcl-x L protein expression were unchanged by exposure to hepcidin; however, the proportion of the anti-apoptotic protein pBad was decreased approximately 50%. A recent report has demonstrated that hepcidin reduces macrophage iron efflux by binding to the iron transporter ferroportin, causing its internalization and subsequent degradation. It is unlikely that the inhibition of CFU-E Colony Formation reported here results from this effect: although macrophages are present in the marrow cell population, and iron is required for erythropoiesis in vitro, the amount of iron-saturated transferrin contributed to the culture medium by FCS is comparable to the amount required for maximal CFU-E Colony Formation in serum-free medium. CONCLUSION: At reduced rhEPO concentrations, CFU-E Colony Formation is inhibited by hepcidin. Short-term exposure to hepcidin induces a pro-apoptotic pattern in HCD57 erythroleukemia cells. The studies reported here do not disprove the possibility that hepcidin-induced impairment of iron flow to erythroid cells contributes to ACD: rather, they suggest an additional mechanism by which hepcidin can inhibit erythropoiesis.
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Effects of Hepcidin, Ferritin, and Iron Deprivation on Erythroid Colony Formation in Vitro.
Blood, 2004Co-Authors: Robert T. Means, Gail Dallalio, Thomas W. FleuryAbstract:The anemia of chronic disease (ACD) results from a combination of three pathologic processes. In ACD, a modest shortening of red cell survival creates an increased demand for red cell production, which is not met because of an impaired erythropoietic response and defects in reticuloendothelial iron mobilization and utilization. The impaired erythropoietic response, in turn, has two components: a blunted erythropoietin response, and an impaired response of erythroid progenitors to erythropoietin. Recombinant human erythropoietin (rhEPO) can reverse this impaired progenitor response in vitro, and can also correct ACD in patients. These processes have generally been considered effects of the cytokines which mediate the immune and inflammatory response, such as tumor necrosis factor, interleukin-1, and the interferons. It has recently been proposed that hepcidin, a mediator of innate immunity with the iron regulatory properties, is the factor responsible for ACD. If this is the case, then hepcidin should be able to induce the pathophysiologic mechanisms implicated in ACD. We therefore evaluated the effects of hepcidin and associated phenomena on human CFU-E Colony Formation in vitro. All CFU-E cultures were performed in plasma clots in serum-containing medium with rhEPO 1 U/mL. Hepcidin at concentrations 10 ng/mL -10 μg/mL had no effect on CFU-E Colony Formation. A number of studies have demonstrated that increased hepcidin message expression and protein production are strongly associated with increases in serum ferritin concentrations, and so the effect of added ferritin on erythroid Colony Formation was studied. Neither ferritin nor apo-ferritin 10 – 1000 ng/mL had inhibitory effects on CFU-E Colony Formation. The effect of iron deprivation on erythroid Colony Formation was evaluated with using desferrioxamine. Desferrioxamine 0.01mM decreased CFU-E Colony Formation to 60% of control values, while higher concentrations completely ablated Colony growth. In summary, hepcidin does not appear to inhibit CFU-E Colony Formation directly or indirectly through ferritin. It may exert such an effect by decreasing availability of iron for erythropoiesis; however, such a finding would be difficult to reconcile with the observed clinical response of ACD to rhEPO, given that iron availability is typically a limiting factor in the erythropoietic response to rhEPO. The role of hepcidin in the overall pathogenesis of ACD remains to be fully determined.
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Thrombospondin enhances erythroid Colony Formation in vitro
Experimental Hematology, 2000Co-Authors: A. Van Laer, Gail Dallalio, Robert T. MeansAbstract:Abstract The thrombospondin (TSP) receptor CD36 is expressed on erythroid progenitors, but only at the erythroid Colony-forming unit (CFU-E) stage. The roles of TSP and CD36 in erythroid development are not well understood. In order to investigate these roles, human bone marrow mononuclear cells (BMMC) were co-cultured in vitro with Chinese hamster ovary (CHO) cells expressing surface CD36. CFU-E Colony Formation was significantly decreased in the presence of CHO-CD36 cells compared to control CHO cells, suggesting that competition for TSP (or some other CD36 ligand) impairs CFU-E Colony Formation. In order to confirm the role of CD36 in this effect, BMMC were cultured with an antibody (FA6-152) which has been reported to activate CD36 signal transduction. FA6-152 significantly increased CFU-E Colony Formation. In order to confirm that this effect involved TSP and not some other CD36 ligand, a dose-response curve with exogenous TSP was performed. In serum-containing cultures, exogenous TSP did not alter CFU-E Colony Formation. However, in serum-free, TSP-deficient, cultures, CFU-E Colony Formation was enhanced by exogenous TSP. At low concentrations of exogenous TSP, the effects of TSP and FA6-152 on Colony Formation were additive. These findings indicate a contribution of TSP and CD36 to late erythroid progenitor development, and provide evidence that these effects are mediated through CD36.
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Inhibition of human erythroid Colony Formation by ceramide
Experimental Hematology, 1999Co-Authors: Gail Dallalio, Melissa North, Bradley D. Worden, Robert T. MeansAbstract:In previous studies, we have demonstrated that the inhibitory effects of tumor necrosis factor (TNF) and interleukin (IL)-1 on human erythroid Colony Formation are indirect and mediated by beta and gamma interferon (IFN), respectively, which act directly upon erythroid Colony forming units (CFU-E). The in vitro inhibitory effect of gammaIFN but not betaIFN is reversed by exposure to high concentrations of recombinant human (rh) erythropoietin (EPO). Ceramide, a product of sphingomyelin hydrolysis, is a known mediator of apoptotic effects of TNF, IL-1, and gammaIFN. In this report, the effects of ceramide on CFU-E Colony Formation and its implication in the model described above are evaluated. Endogenous ceramide produced by exposure to bacterial sphingomyelinase (0.2-2.0 U/mL) and exogenous cell-permeable ceramide (C2-ceramide; 5 and 10 mM) significantly inhibited bone marrow CFU-E Colony Formation. This effect was reversed by the ceramide antagonist sphingosine-1-phosphate (S-1-P). Inhibition of CFU-E by rhgammaIFN, but not rhbetaIFN, was significantly reversed by S-1-P. rhEPO 10 U/mL reversed CFU-E inhibition by C2-ceramide 10 mM. Exposure of marrow cells to rhgammaIFN led to a 57% increase in ceramide content. The present study demonstrates that Colony Formation by human CFU-E is inhibited by endogenous and exogenous ceramide, and that inhibition by rhgammaIFN can be reversed by the ceramide antagonist S-1-P. Inhibition of CFU-E Colony Formation by ceramide and by are both reversed by high concentrations of rhEPO. These findings strongly suggest that ceramide mediates inhibition of human CFU-E Colony Formation by gammaIFN.
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Inhibition of marrow CFU-E Colony Formation from human immunodeficiency virus-infected patients by β- and γ-interferon
American Journal of Hematology, 1996Co-Authors: Gail Dallalio, Melissa North, Robert T. MeansAbstract:: Increased production of cytokines such as beta-interferon (IFN) and gamma-IFN may contribute to the anemia frequently observed in patients with human immunodeficiency virus (HIV) infection. The hypothesis that HIV infection might enhance the susceptibility of erythroid progenitors to cytokine-mediated inhibition was evaluated by comparing the effects of beta- and gamma-IFN on in vitro Colony Formation by marrow erythroid Colony-forming units (CFU-E) from HIV patients, normal volunteers, and anemic non-HIV-infected individuals. CFU-E Colony Formation from HIV patients was not significantly different from controls, and the degree of inhibition by IFN did not differ among patient subsets. HIV infection does not appear to impair baseline CFU-E Colony Formation, nor does it appear to enhance the susceptibility of CFU-E to suppression by cytokines.
Colin S Reynolds - One of the best experts on this subject based on the ideXlab platform.
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Colony Formation in the cyanobacterium microcystis
Biological Reviews, 2018Co-Authors: Man Xiao, Ming Li, Colin S ReynoldsAbstract:Morphological evolution from a unicellular to multicellular state provides greater opportunities for organisms to attain larger and more complex living forms. As the most common freshwater cyanobacterial genus, Microcystis is a unicellular microorganism, with high phenotypic plasticity, which forms colonies and blooms in lakes and reservoirs worldwide. We conducted a systematic review of field studies from the 1990s to 2017 where Microcystis was dominant. Microcystis was detected as the dominant genus in waterbodies from temperate to subtropical and tropical zones. Unicellular Microcystis spp. can be induced to form colonies by adjusting biotic and abiotic factors in laboratory. Colony Formation by cell division has been induced by zooplankton filtrate, high Pb2+ concentration, the presence of another cyanobacterium (Cylindrospermopsis raciborskii), heterotrophic bacteria, and by low temperature and light intensity. Colony Formation by cell adhesion can be induced by zooplankton grazing, high Ca2+ concentration, and microcystins. We hypothesise that single cells of all Microcystis morphospecies initially form colonies with a similar morphology to those found in the early spring. These colonies gradually change their morphology to that of M. ichthyoblabe, M. wesenbergii and M. aeruginosa with changing environmental conditions. Colony Formation provides Microcystis with many ecological advantages, including adaption to varying light, sustained growth under poor nutrient supply, protection from chemical stressors and protection from grazing. These benefits represent passive tactics responding to environmental stress. Microcystis colonies form at the cost of decreased specific growth rates compared with a unicellular habit. Large Colony size allows Microcystis to attain rapid floating velocities (maximum recorded for a single Colony, ∼ 10.08 m h−1) that enable them to develop and maintain a large biomass near the surface of eutrophic lakes, where they may shade and inhibit the growth of less-buoyant species in deeper layers. Over time, accompanying species may fail to maintain viable populations, allowing Microcystis to dominate. Microcystis blooms can be controlled by artificial mixing. Microcystis colonies and non-buoyant phytoplankton will be exposed to identical light conditions if they are evenly distributed over the water column. In that case, green algae and diatoms, which generally have a higher growth rate than Microcystis, will be more successful. Under such mixing conditions, other phytoplankton taxa could recover and the dominance of Microcystis would be reduced. This review advances our understanding of the factors and mechanisms affecting Microcystis Colony Formation and size in the field and laboratory through synthesis of current knowledge. The main transition pathways of morphological changes in Microcystis provide an example of the phenotypic plasticity of organisms during morphological evolution from a unicellular to multicellular state. We emphasise that the mechanisms and factors influencing competition among various close morphospecies are sometimes paradoxical because these morphospecies are potentially a single species. Further work is required to clarify the Colony-forming process in different Microcystis morphospecies and the seasonal variation in this process. This will allow researchers to grow laboratory cultures that more closely reflect field morphologies and to optimise artificial mixing to manage blooms more effectively.