Adhesion Molecule LFA-1/ICAM-1 Influences on LPS-induced Megakaryocytic Emperipolesis in the Rat Bone Marrow

1997 ◽  
Vol 34 (5) ◽  
pp. 463-466 ◽  
Author(s):  
M. Tanaka ◽  
Y. Aze ◽  
T. Fujita
Keyword(s):  
Bone Marrow ◽  
Single Dose ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Flow Cytometric Analysis ◽  
Intercellular Adhesion Molecule ◽  
Lymphocyte Function ◽  
Intercellular Adhesion Molecule 1 ◽  
Flow Cytometric ◽  
Daily Dose

To investigate the effect of adhesion molecules on the occurrence of megakaryocytic emperipolesis of neutrophils, we examined the expression of lymphocyte function-associated antigen 1 (LFA-1) and intercellular adhesion molecule 1 (ICAM-1) in the bone marrow of lipopolysaccharide (LPS)-treated rats (experiment I) and the occurrence of megakaryocytic emperipolesis in anti-LFA-1 antibody-treated rats (experiment II). In experiment I, rats were injected with LPS intravenously at a daily dose of 0.5 mg/kg for 3 days. ICAM-1 was intensely stained on megakaryocytes in LPS-treated rats, as detected by flow cytometric analysis. ICAM-1 was immunostained in the megakaryocytes showing emperipolesis. LFA-1 was immunostained in the neutrophils engulfed by megakaryocytes. In experiment II, rats received anti-LFA-1 antibody intravenously at a single dose of 3 mg/kg. One hour after treatment, rats were given LPS intravenously at a single dose of 0.5 mg/kg. The incidence of megakaryocytic emperipolesis was markedly lower in the anti-LFA-1 antibody + LPS group than in the LPS alone group. These findings suggest that the occurrence of megakaryocytic emperipolesis is partly dependent on adhesion molecules via LFA-1/ICAM-1.

scholarly journals Interleukin-4 Induces Homotypic Aggregation of Human Mast Cells by Promoting LFA-1/ICAM-1 Adhesion Molecules

Blood ◽  
1997 ◽  
Vol 89 (9) ◽  
pp. 3296-3302 ◽  
Author(s):  
Hano Toru ◽  
Tatsuo Kinashi ◽  
Chisei Ra ◽  
Shigeaki Nonoyama ◽  
Jun-ichi Yata ◽  
...  
Keyword(s):  
Mast Cells ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Mononuclear Cells ◽  
Flow Cytometric Analysis ◽  
Interleukin 4 ◽  
Intercellular Adhesion Molecule ◽  
Cellular Interaction ◽  
Lymphocyte Function ◽  
Human Mast Cells

Abstract We report here that interleukin-4 (IL-4) induces homotypic aggregation of cultured human mast cells, grown from cord blood mononuclear cells in the presence of stem cell factor and IL-6. This aggregation was specifically induced by IL-4, because other cytokines including IL-1α, IL-1β, IL-2, IL-3, IL-5, IL-9, IL-10, interferon-γ, IL-12, granulocyte-macrophage colony-stimulating factor, NGF-β, and tumor necrosis factor-α failed to show such effect. Flow cytometric analysis of the cultured mast cells showed that IL-4 increases the expression of lymphocyte function-associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1), but not of very late antigen (VLA) family adhesion molecules or vascular cell adhesion molecule-1 (VCAM-1). Neutralizing monoclonal antibodies specific for LFA-1α, LFA-1β, or ICAM-1 inhibited the IL-4–induced homotypic aggregation of the mast cells, indicating that the aggregation was mediated mainly by LFA-1/ICAM-1 interaction. In addition, IL-4–treated but not untreated mast cells bound to immobilized ICAM-1. This binding was also inhibited by anti-LFA-1 or anti-ICAM-1. These results show that IL-4 promotes expression of ICAM-1 and LFA-1 molecules on mast cells, and suggest that IL-4 may contribute to the migration of mast cells into the inflamed tissue and to the cellular interaction with other inflammatory cells by upregulating adhesion molecules.

Lack of the adhesion molecules P-selectin and intercellular adhesion molecule-1 accelerate the development of BCR/ABL-induced chronic myeloid leukemia-like myeloproliferative disease in mice

Blood ◽  
2004 ◽  
Vol 104 (7) ◽  
pp. 2163-2171 ◽  
Author(s):  
Shawn D. Pelletier ◽  
Daniel S. Hong ◽  
Yiguo Hu ◽  
Yuhua Liu ◽  
Shaoguang Li
Keyword(s):  
Bone Marrow ◽  
Chronic Myeloid Leukemia ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Myeloid Leukemia ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Adhesion Properties ◽  
Marrow Stroma

Abstract In vitro studies show that BCR/ABL-expressing hematopoietic cells exhibit altered adhesion properties. No in vivo studies show whether the altered adhesion properties affect BCR/ABL leukemo-genesis. Using mice with homozygous inactivation of genes encoding the 2 adhesion molecules P-selectin and intercellular adhesion molecule-1 (ICAM1), we show that the mutant mice develop BCR/ABL-induced chronic myeloid leukemia (CML)-like leukemia at a significantly faster rate than do wild-type (WT) mice. Lack of P-selectin and ICAM1 did not have a significant effect on the development of B-cell acute lymphoblastic leukemia (BALL) induced by BCR/ABL. Using mice deficient for P-selectin or ICAM1 alone, we show that P-selectin plays a major role in the acceleration of CML-like leukemia. Lack of P-selectin resulted in early release of BCR/ABL-expressing myeloid progenitors from bone marrow, appearing to alter the biologic properties of leukemic cells rather than their growth rate by increasing their homing to the lungs, causing fatal lung hemorrhages. These results indicate that adhesion of BCR/ABL-expressing myeloid progenitors to marrow stroma through P-selectin and ICAM1 play an inhibitory role in the development of CML-like disease, suggesting that improvement of adhesion between BCR/ABL-expressing myeloid progenitor cells and bone marrow stroma may be of therapeutic value for human CML. (Blood. 2004;104:2163-2171)

scholarly journals Expression of intercellular adhesion molecule-1 (CD54) on hematopoietic progenitors

Blood ◽  
1991 ◽  
Vol 77 (5) ◽  
pp. 948-953 ◽  
Author(s):  
S Arkin ◽  
B Naprstek ◽  
L Guarini ◽  
S Ferrone ◽  
JM Lipton
Keyword(s):  
Bone Marrow ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Lymphocyte Function ◽  
Hematopoietic Tissue ◽  
Intercellular Adhesion Molecule 1 ◽  
Colony Forming Units ◽  
Semi Solid ◽  
Cell Cell

The distribution of intercellular adhesion molecule-1 (ICAM-1), a ligand for lymphocyte function antigen-1, on hematopoietic tissue was determined using the anti-ICAM-1 monoclonal antibody CL203.4 with flow cytometry and short-term semi-solid hematopoietic progenitor cultures. After timed incubation in media with fetal bovine serum, 29% of erythroid burst-forming units (BFU-E), 24% of erythroid colony-forming units (CFU-E), and 52% of granulocyte-macrophage colony-forming units (CFU-GM) bone marrow progenitors expressed ICAM-1. This finding, which is consistent with the detection of ICAM-1 on acute non-lymphoblastic leukemic blasts, is at variance with recent reports. ICAM-1 was also detected on bone marrow blasts, proerythroblasts, promyelocytes, and cells of monocyte/macrophage lineage, but was not detected on erythroblasts, normoblasts, neutrophilic myelocytes, metamyelocytes, bands, or on most lymphocytes. These results indicate that maturation of cells of the erythroid and myeloid lineage is associated with loss of ICAM-1. The distribution of ICAM-1 on bone marrow progenitors, early precursor cells, and accessory cells in conjunction with the function of this molecule in cell-cell interactions suggests that ICAM-1 may play a role in the cell-cell and cell-stromal interactions that regulate hematopoiesis.

scholarly journals Expression of intercellular adhesion molecule-1 (CD54) on hematopoietic progenitors

Blood ◽  
1991 ◽  
Vol 77 (5) ◽  
pp. 948-953 ◽  
Author(s):  
S Arkin ◽  
B Naprstek ◽  
L Guarini ◽  
S Ferrone ◽  
JM Lipton
Keyword(s):  
Bone Marrow ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Lymphocyte Function ◽  
Hematopoietic Tissue ◽  
Intercellular Adhesion Molecule 1 ◽  
Colony Forming Units ◽  
Semi Solid ◽  
Cell Cell

Abstract The distribution of intercellular adhesion molecule-1 (ICAM-1), a ligand for lymphocyte function antigen-1, on hematopoietic tissue was determined using the anti-ICAM-1 monoclonal antibody CL203.4 with flow cytometry and short-term semi-solid hematopoietic progenitor cultures. After timed incubation in media with fetal bovine serum, 29% of erythroid burst-forming units (BFU-E), 24% of erythroid colony-forming units (CFU-E), and 52% of granulocyte-macrophage colony-forming units (CFU-GM) bone marrow progenitors expressed ICAM-1. This finding, which is consistent with the detection of ICAM-1 on acute non-lymphoblastic leukemic blasts, is at variance with recent reports. ICAM-1 was also detected on bone marrow blasts, proerythroblasts, promyelocytes, and cells of monocyte/macrophage lineage, but was not detected on erythroblasts, normoblasts, neutrophilic myelocytes, metamyelocytes, bands, or on most lymphocytes. These results indicate that maturation of cells of the erythroid and myeloid lineage is associated with loss of ICAM-1. The distribution of ICAM-1 on bone marrow progenitors, early precursor cells, and accessory cells in conjunction with the function of this molecule in cell-cell interactions suggests that ICAM-1 may play a role in the cell-cell and cell-stromal interactions that regulate hematopoiesis.

scholarly journals Adhesion-dependent interactions between eosinophils and cholinergic nerves

2002 ◽  
Vol 282 (6) ◽  
pp. L1229-L1238 ◽  
Author(s):  
Paul J. Kingham ◽  
W. Graham McLean ◽  
Deborah A. Sawatzky ◽  
Marie Therese Walsh ◽  
Richard W. Costello
Keyword(s):  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cell Function ◽  
Intercellular Adhesion Molecule ◽  
Cholinergic Nerves ◽  
Intercellular Adhesion Molecule 1 ◽  
Parasympathetic Nerves ◽  
Oxidase Inhibition ◽  
Cell Adhesion Molecule 1 ◽  
Eosinophil Degranulation

Eosinophils adhere to airway cholinergic nerves and influence nerve cell function by releasing granule proteins onto inhibitory neuronal M2 muscarinic receptors. This study investigated the mechanism of eosinophil degranulation by cholinergic nerves. Eosinophils were cocultured with IMR32 cholinergic nerve cells, and eosinophil peroxidase (EPO) or leukotriene C4 (LTC4) release was measured. Coculture of eosinophils with nerves significantly increased EPO and LTC4 release compared with eosinophils alone. IMR32 cells, like parasympathetic nerves, express the adhesion molecules vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 (ICAM-1). Inhibition of these adhesion molecules alone or in combination significantly inhibited eosinophil degranulation. IMR32 cells also significantly augmented the eosinophil degranulation produced by formyl-Met-Leu-Phe. Eosinophil adhesion to IMR32 cells resulted in an ICAM-1-mediated production of reactive oxygen species via a neuronal NADPH oxidase, inhibition of which significantly inhibited eosinophil degranulation. Additionally, eosinophil adhesion increased the release of ACh from IMR32 cells. These neuroinflammatory cell interactions may be relevant in a variety of inflammatory and neurological conditions.

scholarly journals Contribution of lymphocyte function-associated-1/intercellular adhesion molecule-1 binding to the adhesion/signaling cascade of cytotoxic T lymphocyte activation.

1994 ◽  
Vol 179 (1) ◽  
pp. 359-363 ◽  
Author(s):  
B Ybarrondo ◽  
A M O'Rourke ◽  
A A Brian ◽  
M F Mescher
Keyword(s):  
Adhesion Molecule ◽  
Cytotoxic T Lymphocyte ◽  
Lymphocyte Activation ◽  
Cell Receptor ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Lymphocyte Function ◽  
Intercellular Adhesion Molecule 1 ◽  
Rapid Induction ◽  
Blocking Effects

A rapid induction of adhesion to immobilized intercellular adhesion molecule (ICAM)-1 occurs when cytotoxic T lymphocytes (CTL) are stimulated with either soluble anti-T cell receptor (TCR) monoclonal antibodies (mAb) or with immobilized alloantigen, and this binding is blocked by the addition of anti-lymphocyte function-associated (LFA)-1 mAbs. Requirements for activating LFA-1 adhesion to ICAM-1 are similar to those found for induction of binding to immobilized fibronectin (FN), but distinct from those for activating CD8-mediated adhesion to class I major histocompatibility complex. A distinct role for LFA-1 in co-signaling for TCR-dependent degranulation could not be demonstrated. In contrast, both CD8 and the FN-binding integrin provide costimulatory signals for this response. Thus, if co-signaling via LFA-1 occurs, it clearly differs from that provided by CD8 or the FN-binding integrin. On the basis of antibody blocking effects, alloantigen-dependent activation of adhesion to ICAM-1 involves both the TCR and CD8. These results support a view of CTL activation as a cascade of adhesion and signaling events, with different coreceptors making distinct contributions.

scholarly journals Metformin Sensitizes Leukemic Cells to Cytotoxic Lymphocytes by Increasing Expression of Intercellular Adhesion Molecule-1 (ICAM-1)

2021 ◽  
Author(s):  
Nerea Allende-Vega ◽  
Joaquin Marco Brualla ◽  
Paolo Falvo ◽  
Catherine Alexia ◽  
Michael Constantinides ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Adhesion Molecule ◽  
Tumor Antigens ◽  
Intercellular Adhesion ◽  
Leukemic Cells ◽  
Intercellular Adhesion Molecule ◽  
Cytotoxic Lymphocytes ◽  
Lymphocyte Function ◽  
Intercellular Adhesion Molecule 1 ◽  
Cytotoxic Lymphocyte

Abstract Solid tumor cells have an altered metabolism that can protect them from cytotoxic lymphocytes. The antidiabetic drug metformin modifies tumor cell metabolism and several clinical trials are testing its effectiveness for the treatment of solid cancers. The use of metformin in hematologic cancers has received much less attention, although allogeneic cytotoxic lymphocytes are very effective against these tumors. We show here that metformin induces expression of Natural Killer G2-D (NKG2D) ligands (NKG2DL) and intercellular adhesion molecule-1 (ICAM-1), a ligand of the lymphocyte function-associated antigen 1 (LFA-1). This leads to enhance sensitivity to cytotoxic lymphocytes. Overexpression of antiapoptotic Bcl-2 family members decrease both metformin effects. The sensitization to activated cytotoxic lymphocytes is mainly mediated by the increase on ICAM-1 levels, which favors cytotoxic lymphocytes binding to tumor cells. Finally, metformin decreases the growth of human hematological tumor cells in xenograft models, mainly in presence of monoclonal antibodies that recognize tumor antigens. Our results suggest that metformin could improve cytotoxic lymphocyte-mediated therapy.

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