scholarly journals Taro Lectin Can Act as a Cytokine-Mimetic Compound, Stimulating Myeloid and T Lymphocyte Lineages and Protecting Progenitors in Murine Bone Marrow

Pharmaceutics ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 350
Author(s):  
Erika Bertozzi de Aquino Mattos ◽  
Patricia Ribeiro Pereira ◽  
Lyris Anunciata Demétrio Mérida ◽  
Anna Carolina Nitzsche Teixeira Fernandes Corrêa ◽  
Maria Paula Vigna Freire ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Cell Lineage ◽  
Hematopoietic Progenitor Cell ◽  
Dependent Manner ◽  
Relative Percentage ◽  
Murine Bone Marrow ◽  
Gm Csf ◽  
Csf Cells ◽  
Progenitor Cell Proliferation

Taro (Colocasia esculenta) corm is traditionally consumed as a medicinal plant to stimulate immune responses and restore a health status. Tarin, a taro lectin, is considered responsible for the immunomodulatory effects of taro. In the present study, in order to investigate the effects of tarin on bone marrow hematopoietic population, murine cells were stimulated with tarin combined with a highly enriched conditioned medium containing either IL-3 or GM-CSF. Cells challenged with tarin proliferated in a dose-dependent manner, evidenced by the increase in cell density and number of clusters and colonies. Tarin exhibited a cytokine-mimetic effect similar to IL-3 and GM-CSF, increasing granulocytic cell lineage percentages, demonstrated by an increase in the relative percentage of Gr-1+ cells. Tarin does not increase lymphocytic lineages, but phenotyping revealed that the relative percentage of CD3+ cells was increased with a concomitant decrease in CD19+ and IL-7Rα+ cells. Most bone marrow cells were stained with tarin-FITC, indicating non-selective tarin binding, a phenomenon that must still be elucidated. In conclusion, taro corms contain an immunomodulatory lectin able to boost the immune system by promoting myeloid and lymphoid hematopoietic progenitor cell proliferation and differentiation.

scholarly journals Small-molecule inhibitor sorafenib regulates immunoreactions by inducing survival and differentiation of bone marrow cells

2016 ◽  
Vol 22 (7) ◽  
pp. 493-502 ◽  
Author(s):  
Xiangxuan Zhao ◽  
Mengde Cao ◽  
Zaiming Lu ◽  
Ton Wang ◽  
Ying Ren ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cells ◽  
Liver Cancer ◽  
Bone Marrow Cells ◽  
Dependent Manner ◽  
Low Doses ◽  
Murine Bone Marrow ◽  
Immunosuppressive Cell ◽  
Murine Liver ◽  
Marrow Cells

Sorafenib has been used for the treatment of liver cancer. However, its clinical impact on human immunity system remains poorly known. Our previous study has shown that sorafenib modulates immunosuppressive cell populations in murine liver cancer models. Here, we continue to report that low doses of sorafenib promotes the survival of murine bone marrow cells (BMCs) in a dose-dependent manner by up-regulating the anti-apoptotic protein survivin. Sorafenib induces differentiation of BMCs into suppressive dendritic cells that inhibit autologous T-cell proliferation and stimulate CD4+ T cells to express increased IL-1β, IL-2, IL-4, IL-10, IFN-γ and TNF-α, and reduced levels of IL-6 and CD25, which indicates that sorafenib-induced dendritic cells represent a distinct cellular subset with unique properties. Taken together, our findings suggest that in addition to its anticancer effects, sorafenib has an immunoregulatory property that is apparent at low doses.

scholarly journals FcγRII (CD32) Is Linked to Apoptotic Pathways in Murine Granulocyte Precursors and Mature Eosinophils

Blood ◽  
1997 ◽  
Vol 90 (3) ◽  
pp. 1267-1274 ◽  
Author(s):  
Belen de Andrés ◽  
Allen L. Mueller ◽  
Arthur Blum ◽  
Joel Weinstock ◽  
Sjef Verbeek ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Tissue Injury ◽  
Chromatin Condensation ◽  
Annexin V ◽  
Murine Bone Marrow ◽  
Gm Csf ◽  
Bone Marrow Cultures ◽  
Macrophage Colony ◽  
Apoptotic Pathways

Murine granulocytes and precursors express low-affinity IgG Fc receptors (FcγR). We investigated the effects of FcγR ligation on the development of eosinophils in cultures of normal murine bone marrow. Eosinophilopoiesis was induced by culture of bone marrow cells in the presence of cytokines (granulocyte-macrophage colony-stimulating factor [GM-CSF], interleukin-3 [IL-3], and IL-5). Addition to the cultures of 2.4G2, a rat monoclonal antibody (mAb) that reacts with FcγRII (CD32) and FcγRIII (CD16), induced granulocyte apoptosis within 24 hours. Granulocytes in cultures that contained 2.4G2 showed chromatin condensation, binding of Annexin-V, and fas induction, and by electron microscopy, apoptosis was most commonly observed in cells of the eosinophil lineage. Since murine granulocytes can express both FcγRII (CD32) and FcγRIII (CD16), we investigated the effect of 2.4G2 on cultures of bone marrow obtained from FcγRIII (CD16) gene–disrupted mice and found that the apoptosis induced with 2.4G2 was CD16-independent. Studies with bone marrow cultures from B6MLR-lpr/lpr and C3H/HEJ-gld/gld mice established that the FcγRII (CD32)-triggered apoptosis was fas-fasL–dependent. When mature eosinophils isolated from hepatic granulomas of Schistosoma mansoni–infected mice were cultured in cytokines in the presence of 2.4G2, the eosinophils underwent apoptosis within 24 hours. These findings identify a previously unknown linkage between FcγR on eosinophils and fas-mediated apoptosis, a connection that could be relevant to mechanisms by which eosinophils mediate tissue injury and antibody-dependent cellular cytotoxicity reactions.

scholarly journals A stimulatory effect of recombinant murine interleukin-7 (IL-7) on B- cell colony formation and an inhibitory effect of IL-1 alpha

Blood ◽  
1989 ◽  
Vol 74 (6) ◽  
pp. 1936-1941 ◽  
Author(s):  
T Suda ◽  
S Okada ◽  
J Suda ◽  
Y Miura ◽  
M Ito ◽  
...  
Keyword(s):  
Bone Marrow ◽  
B Cell ◽  
Colony Formation ◽  
Bone Marrow Cells ◽  
Dependent Manner ◽  
Reciprocal Effect ◽  
Gm Csf ◽  
Interleukin 7 ◽  
Cell Colony ◽  
Marrow Cells

Abstract Using a clonal culture system, we investigated the lymphohematopoietic effects of recombinant interleukin-7 (IL-7) obtained from conditioned media of transfected COS 1 cells. IL-7 alone acted on murine bone marrow cells and supported the formation of B-cell colonies. These colony cells were positive for B220, and some of them were also found to have either IgM or Thy-1. B220+, IgM- cells, but not B220- cells sorted from fresh bone marrow cells were able to form B cell colonies in the presence of IL-7. Thus, IL-7 supported the differentiation of B220+, IgM- cells to B220+, IgM+ cells. B220+, IgM+ cells did not proliferate in the presence of IL-7. IL-7 did not affect the myeloid colony formation supported by IL-3, IL-5, IL-6, granulocyte macrophage colony stimulating factor (GM-CSF), and G-CSF. On the other hand, lymphocyte colony formation was not affected by IL-2, IL-3, IL-4, IL-5, IL-6, GM-CSF, or G-CSF. Interestingly, IL-1 alpha inhibited IL-7- induced B cell colony formation in a dose-dependent manner, while the same concentration of IL-1 alpha enhanced the myeloid colony formation by IL-3. This reciprocal effect of IL-1 alpha may act on hematopoietic progenitor cells without accessory cells. These data show that IL-7 is a B cell growth factor and that IL-1 alpha may play an important role in differentiation of myeloid and lymphoid lineages.

scholarly journals Macrophage colony-stimulating factor-induced bone marrow macrophages do not synthesize or release prostaglandin E2

Blood ◽  
1994 ◽  
Vol 83 (11) ◽  
pp. 3316-3323 ◽  
Author(s):  
Y Shibata ◽  
DR Bjorkman ◽  
M Schmidt ◽  
Y Oghiso ◽  
A Volkman
Keyword(s):  
Bone Marrow ◽  
Enzyme Activity ◽  
Prostaglandin E2 ◽  
Bone Marrow Cells ◽  
Mrna Levels ◽  
Colony Stimulating Factor ◽  
Murine Bone Marrow ◽  
Gm Csf ◽  
Stimulating Factor

Abstract Previously, we found that murine bone marrow-derived macrophages (MO) induced in vitro by MO-specific colony-stimulating factor (M-CSF) have little capacity to release prostaglandin E2 (PGE2) and other eicosanoids. This work focused on the functional and transcriptional expression of the key enzymes for the PGE2 synthesis in the MO. Nonadherent bone marrow cells were cultured with RPMI1640 plus 10% fetal bovine serum (FBS) further supplemented with either M-CSF or granulocyte-macrophage (GM)-CSF and interleukin-3 (IL-3). Cellular PGG/H synthase (cyclooxygenase) levels were quantified by cytometric analysis with antibodies specific for the two isozymes of PGG/H synthase (PGG/H synthases 1 and 2). The enzyme activity was monitored by adding exogenous arachidonic acid (AA) substrate to the bone marrow MO cultures and to the cell-free particulate fractions. The levels of PGE2 converted were quantitated by radioimmunoassay (RIA). mRNA levels of the enzymes were detected by Northern blot analysis hybridized with mouse PGG/H synthase cDNA probes, 2.7 kb (PGG/H synthase 1) and 4.2 kb (PGG/H synthase 2). In addition, cellular phospholipase A2 (PLA2) activities were detected with sn-2–14C-arachidonyl phosphatidylcholine as a substrate. Cells proliferating in the presence of GM-CSF and IL-3 for more than 4 days showed significant release of PGE2 (> 7 ng/10(6) cells) when stimulated by AA. These cells also expressed significant amounts of PGG/H synthase 1 protein, its mRNA (2.7 kb) and cellular PLA2. M-CSF-induced MO, in sharp contrast, expressed little PGG/H synthase protein, mRNA, cellular enzyme activity, or PGE2 release, despite comparable levels of cellular PLA2 activity. These data suggest that the capacity of differentiating marrow-derived MO to form PGE2 is growth factor-dependent.

scholarly journals A stimulatory effect of recombinant murine interleukin-7 (IL-7) on B- cell colony formation and an inhibitory effect of IL-1 alpha

Blood ◽  
1989 ◽  
Vol 74 (6) ◽  
pp. 1936-1941 ◽  
Author(s):  
T Suda ◽  
S Okada ◽  
J Suda ◽  
Y Miura ◽  
M Ito ◽  
...  
Keyword(s):  
Bone Marrow ◽  
B Cell ◽  
Colony Formation ◽  
Bone Marrow Cells ◽  
Dependent Manner ◽  
Reciprocal Effect ◽  
Gm Csf ◽  
Interleukin 7 ◽  
Cell Colony ◽  
Marrow Cells

Using a clonal culture system, we investigated the lymphohematopoietic effects of recombinant interleukin-7 (IL-7) obtained from conditioned media of transfected COS 1 cells. IL-7 alone acted on murine bone marrow cells and supported the formation of B-cell colonies. These colony cells were positive for B220, and some of them were also found to have either IgM or Thy-1. B220+, IgM- cells, but not B220- cells sorted from fresh bone marrow cells were able to form B cell colonies in the presence of IL-7. Thus, IL-7 supported the differentiation of B220+, IgM- cells to B220+, IgM+ cells. B220+, IgM+ cells did not proliferate in the presence of IL-7. IL-7 did not affect the myeloid colony formation supported by IL-3, IL-5, IL-6, granulocyte macrophage colony stimulating factor (GM-CSF), and G-CSF. On the other hand, lymphocyte colony formation was not affected by IL-2, IL-3, IL-4, IL-5, IL-6, GM-CSF, or G-CSF. Interestingly, IL-1 alpha inhibited IL-7- induced B cell colony formation in a dose-dependent manner, while the same concentration of IL-1 alpha enhanced the myeloid colony formation by IL-3. This reciprocal effect of IL-1 alpha may act on hematopoietic progenitor cells without accessory cells. These data show that IL-7 is a B cell growth factor and that IL-1 alpha may play an important role in differentiation of myeloid and lymphoid lineages.

scholarly journals FcγRII (CD32) Is Linked to Apoptotic Pathways in Murine Granulocyte Precursors and Mature Eosinophils

Blood ◽  
1997 ◽  
Vol 90 (3) ◽  
pp. 1267-1274 ◽  
Author(s):  
Belen de Andrés ◽  
Allen L. Mueller ◽  
Arthur Blum ◽  
Joel Weinstock ◽  
Sjef Verbeek ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Tissue Injury ◽  
Chromatin Condensation ◽  
Annexin V ◽  
Murine Bone Marrow ◽  
Gm Csf ◽  
Bone Marrow Cultures ◽  
Macrophage Colony ◽  
Apoptotic Pathways

Abstract Murine granulocytes and precursors express low-affinity IgG Fc receptors (FcγR). We investigated the effects of FcγR ligation on the development of eosinophils in cultures of normal murine bone marrow. Eosinophilopoiesis was induced by culture of bone marrow cells in the presence of cytokines (granulocyte-macrophage colony-stimulating factor [GM-CSF], interleukin-3 [IL-3], and IL-5). Addition to the cultures of 2.4G2, a rat monoclonal antibody (mAb) that reacts with FcγRII (CD32) and FcγRIII (CD16), induced granulocyte apoptosis within 24 hours. Granulocytes in cultures that contained 2.4G2 showed chromatin condensation, binding of Annexin-V, and fas induction, and by electron microscopy, apoptosis was most commonly observed in cells of the eosinophil lineage. Since murine granulocytes can express both FcγRII (CD32) and FcγRIII (CD16), we investigated the effect of 2.4G2 on cultures of bone marrow obtained from FcγRIII (CD16) gene–disrupted mice and found that the apoptosis induced with 2.4G2 was CD16-independent. Studies with bone marrow cultures from B6MLR-lpr/lpr and C3H/HEJ-gld/gld mice established that the FcγRII (CD32)-triggered apoptosis was fas-fasL–dependent. When mature eosinophils isolated from hepatic granulomas of Schistosoma mansoni–infected mice were cultured in cytokines in the presence of 2.4G2, the eosinophils underwent apoptosis within 24 hours. These findings identify a previously unknown linkage between FcγR on eosinophils and fas-mediated apoptosis, a connection that could be relevant to mechanisms by which eosinophils mediate tissue injury and antibody-dependent cellular cytotoxicity reactions.

scholarly journals TLR5 signaling in murine bone marrow induces hematopoietic progenitor cell proliferation and aids survival from radiation

2017 ◽  
Vol 1 (21) ◽  
pp. 1796-1806 ◽  
Author(s):  
Benyue Zhang ◽  
Damilola Oyewole-Said ◽  
Jun Zou ◽  
Ifor R. Willliams ◽  
Andrew T. Gewirtz
Keyword(s):  
Bone Marrow ◽  
Cell Proliferation ◽  
Progenitor Cell ◽  
Hematopoietic Progenitor Cell ◽  
Mouse Bone Marrow ◽  
Hematopoietic Progenitor ◽  
Murine Bone Marrow ◽  
Key Points ◽  
Progenitor Cell Proliferation ◽  
Lethal Irradiation

Key Points Flagellin activates TLR5 signaling in mouse bone marrow and induces hematopoietic progenitor cell proliferation. Flagellin-induced MPP3 cells aid the survival of mice exposed to lethal irradiation.

Identifying Downstream Targets of HOXB4 Using the EML Primitive Hematopoietic Progenitor Cell Line.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4150-4150
Author(s):  
Han M. Lee ◽  
Hui Zhang ◽  
Bernard G. Forget
Keyword(s):  
Bone Marrow ◽  
Cell Line ◽  
Bone Marrow Cells ◽  
Ex Vivo ◽  
Differentially Expressed ◽  
Hematopoietic Progenitor Cell ◽  
Competitive Growth ◽  
Murine Bone Marrow ◽  
Downstream Targets

Abstract Ectopic expression of the homeobox transcription factor HOXB4 has been shown to enhance hematopoietic stem cell (HSC) self-renewal and expansion ex vivo and in vivo. Murine bone marrow transplantation experiments have also shown that overexpression of HOXB4 in HSCs confers a competitive repopulation advantage in vivo. Identifying the largely unknown downstream targets of HOXB4 would be beneficial in understanding the molecular mechanisms associated with HSC self-renewal and expansion. In order to identify the downstream targets of HOXB4, we have constitutively overexpressed HOXB4 in the primitive hematopoietic progenitor cell line, EML, by transduction of the cells with the MSCV-HOXB4-IRES-GFP retroviral vector used by workers in studies of primary murine bone marrow cells. Similar to the results from ex vivo and in vivo experiments with primary bone marrow cells, we found that HOXB4 overexpression conferred a competitive growth advantage to EML cells compared to EML cells expressing GFP alone. However, as the EML cells overexpressing HOXB4 were maintained in culture, the competitive growth advantage disappeared over time and was completely lost after 3 months of continuous culture. No abnormal block to differentiation was observed when EML cells overexpressing HOXB4 were stimulated by ATRA + IL3 to differentiate along the granulocyte/macrophage pathway to produce the more mature GM-CSF-dependent cell line designated EPRO (EML-derived promyelocytes). Our analysis showed that HOXB4 was still being overexpressed in the EPRO cells and that this overexpression did not give the EPRO cells a competitive growth advantage. This finding suggests that HOXB4 gives a competitive growth advantage only to more primitive EML cells and does not have the same effect on the more mature EPRO cells. The gene expression profile of cells that overexpressed HOXB4 was compared to that of cells transduced with vector alone. Our first set of results from gene expression profile experiments showed that a variety of gene products were differentially expressed at statistically higher or lower levels than in control cells when HOXB4 was overexpressed. In our first analysis using chip A of the Affymetrix U74v2 chip set, a microarray chip containing oligonucleotide probes for over 12,000 gene products, we found that a total of 189 genes were differentially expressed between cells that overexpressed HOXB4 and cells that did not. Most striking was the downregulation by over 30 fold in cells that overexpressed HOXB4 of a mRNA encoding a protein in a pro-apoptotic signaling pathway. Other potentially interesting genes that were differentially expressed included: 10 transcription factors, 6 cell cycle-associated proteins, 2 chemokine receptors and 4 additional apoptosis pathway-related proteins. These findings suggest that the EML cell line is a valid model system to use in elucidating downstream targets of HOXB4. Future studies are being planned to utilize EML cells overexpressing a HOXB4 protein fused to a truncated estrogen receptor (ER) to identify the genes that are direct downstream targets of HOXB4 after short-term induction of HOXB4 activity by tamoxifen.

scholarly journals Macrophage colony-stimulating factor-induced bone marrow macrophages do not synthesize or release prostaglandin E2

Blood ◽  
1994 ◽  
Vol 83 (11) ◽  
pp. 3316-3323 ◽  
Author(s):  
Y Shibata ◽  
DR Bjorkman ◽  
M Schmidt ◽  
Y Oghiso ◽  
A Volkman
Keyword(s):  
Bone Marrow ◽  
Enzyme Activity ◽  
Prostaglandin E2 ◽  
Bone Marrow Cells ◽  
Mrna Levels ◽  
Colony Stimulating Factor ◽  
Murine Bone Marrow ◽  
Gm Csf ◽  
Stimulating Factor

Previously, we found that murine bone marrow-derived macrophages (MO) induced in vitro by MO-specific colony-stimulating factor (M-CSF) have little capacity to release prostaglandin E2 (PGE2) and other eicosanoids. This work focused on the functional and transcriptional expression of the key enzymes for the PGE2 synthesis in the MO. Nonadherent bone marrow cells were cultured with RPMI1640 plus 10% fetal bovine serum (FBS) further supplemented with either M-CSF or granulocyte-macrophage (GM)-CSF and interleukin-3 (IL-3). Cellular PGG/H synthase (cyclooxygenase) levels were quantified by cytometric analysis with antibodies specific for the two isozymes of PGG/H synthase (PGG/H synthases 1 and 2). The enzyme activity was monitored by adding exogenous arachidonic acid (AA) substrate to the bone marrow MO cultures and to the cell-free particulate fractions. The levels of PGE2 converted were quantitated by radioimmunoassay (RIA). mRNA levels of the enzymes were detected by Northern blot analysis hybridized with mouse PGG/H synthase cDNA probes, 2.7 kb (PGG/H synthase 1) and 4.2 kb (PGG/H synthase 2). In addition, cellular phospholipase A2 (PLA2) activities were detected with sn-2–14C-arachidonyl phosphatidylcholine as a substrate. Cells proliferating in the presence of GM-CSF and IL-3 for more than 4 days showed significant release of PGE2 (> 7 ng/10(6) cells) when stimulated by AA. These cells also expressed significant amounts of PGG/H synthase 1 protein, its mRNA (2.7 kb) and cellular PLA2. M-CSF-induced MO, in sharp contrast, expressed little PGG/H synthase protein, mRNA, cellular enzyme activity, or PGE2 release, despite comparable levels of cellular PLA2 activity. These data suggest that the capacity of differentiating marrow-derived MO to form PGE2 is growth factor-dependent.

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