The Experts below are selected from a list of 540 Experts worldwide ranked by ideXlab platform
M Owhashi - One of the best experts on this subject based on the ideXlab platform.
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production of Eosinophil Chemotactic Factor by cd8 t cells in toxocara canis infected mice
Parasitology Research, 1997Co-Authors: M Owhashi, Hiroyuki Arita, A NiwaAbstract:Production of Eosinophil Chemotactic Factor by T-lymphocytes (ECF-L) was examined in Toxocara canis-infected mice. When spleen cells from T. canis-infected mice were cultured in serum-free RPMI1640, ECF-L production was detectable in an antigen-specific manner. The ECF-L production peaked at day 9 post-infection and then decreased. Depletion of Thy 1.2+ cells or CD8+ cells completely abrogated ECF-L production, whereas depletion of CD4+ cells did not, indicating that CD8+ T-cells are involved in the production of ECF-L. When bone marrow Eosinophils obtained from T. canis-infected mice were preincubated with ECF-L, their Chemotactic reactivity to parasite-derived ECFs was enhanced, whereas that of peritoneal cavity-derived Eosinophils was not. Thus, ECF-L seems to be important not only as a chemoattractant but also as an activator of the Chemotactic reactivity of naive Eosinophils to the parasite-derived ECF in T. canis infection.
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kinetic study of Eosinophil Chemotactic Factor production with reference to Eosinophilia and granuloma formation in mice infected with schistosoma japonicum
Parasitology International, 1997Co-Authors: M Owhashi, Haruhiko Maruyama, Yukifumi NawaAbstract:Abstract Kinetic changes of Eosinophil Chemotactic Factor (ECF) production from granulomas, splenic T-cells or mast cells were examined with reference to granuloma formation around newly deposited single eggs in Schistosoma japonicum -infected mice. The peri-ovular granulomas began to appear at around 5 weeks post-infection (p.i.). Their size reached a peak at 6 weeks and then decreased gradually. Up to 8 weeks p.i., Eosinophils were the predominant cell type in the granulomas. ECF-release from isolated granulomas paralleled the size of granulomas. Circulating ECF-A, which was assumed to be derived from mast cells, was also detected 6 weeks afterwards in parallel with the level of specific IgE antibody level against egg antigens in the serum. The circulating ECF-A peaked at 8 weeks and decreased after 10 weeks. Spleen cells began to produce ECF specific to bone-marrow Eosinophils began at 5 weeks p.i., reached a peak at 6 weeks and then decreased rapidly. On the other hand, the production of ECF specific to Eosinophils obtained from the peritoneal cavity began at 6 weeks and decreased rapidly thereafter. These results suggest that various kinds of host-derived ECFs seem to contribute, in one way or an other, to the accumulation of Eosinophils in and around granulomatons lesions. The possible role of these ECFs in Eosinophil mobilization from the site of production to the inflamed site is discussed.
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Eosinophil Chemotactic Factor release from neutrophils induced by stimulation with schistosoma japonicum eggs
Parasitology Research, 1996Co-Authors: M Owhashi, N Kirai, Y HoriiAbstract:The neutrophil is one of the sources of Eosinophil Chemotactic Factor (ECF) in the presence of some stimulants. In the present study we showed that guinea-pig neutrophils could release ECF upon stimulation with Schistosoma japonicum eggs. ECF release from neutrophils began as early as 5 min after the stimulation and reached a peak at 20 min. When homogenate of the eggs was separated into a water-soluble fraction as soluble egg antigen (SEA) and a water-insoluble fraction (eggshell), both preparations possessed a potent neutrophil-stimulating activity to release ECF. The ECF release was dependent on the concentration of eggshells or SEA or on the number of neutrophils. The neutrophil-stimulating activity of eggshells was stable to heat, HCl, or pronase treatment but sensitive to NaOH treatment. When the eggs or eggshells were washed with acetone or Tween-20, they lost the neutrophil-stimulating activity to release ECF, indicating that the neutrophil-stimulating Factor (NSF) possesses a lipid nature. The molecular weight of NSF extracted from the eggshells was estimated to be about 1000 Da by gel chromatography on Sephadex G25. The possible role of eggshells in the formation of Eosinophil-rich granulomatous lesions in schistosomiasis japonica is discussed.
Y Horii - One of the best experts on this subject based on the ideXlab platform.
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Eosinophil Chemotactic Factor release from neutrophils induced by stimulation with schistosoma japonicum eggs
Parasitology Research, 1996Co-Authors: M Owhashi, N Kirai, Y HoriiAbstract:The neutrophil is one of the sources of Eosinophil Chemotactic Factor (ECF) in the presence of some stimulants. In the present study we showed that guinea-pig neutrophils could release ECF upon stimulation with Schistosoma japonicum eggs. ECF release from neutrophils began as early as 5 min after the stimulation and reached a peak at 20 min. When homogenate of the eggs was separated into a water-soluble fraction as soluble egg antigen (SEA) and a water-insoluble fraction (eggshell), both preparations possessed a potent neutrophil-stimulating activity to release ECF. The ECF release was dependent on the concentration of eggshells or SEA or on the number of neutrophils. The neutrophil-stimulating activity of eggshells was stable to heat, HCl, or pronase treatment but sensitive to NaOH treatment. When the eggs or eggshells were washed with acetone or Tween-20, they lost the neutrophil-stimulating activity to release ECF, indicating that the neutrophil-stimulating Factor (NSF) possesses a lipid nature. The molecular weight of NSF extracted from the eggshells was estimated to be about 1000 Da by gel chromatography on Sephadex G25. The possible role of eggshells in the formation of Eosinophil-rich granulomatous lesions in schistosomiasis japonica is discussed.
Judith E Allen - One of the best experts on this subject based on the ideXlab platform.
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A Brugia malayi Homolog of Macrophage Migration Inhibitory Factor Reveals an Important Link Between Macrophages and
2014Co-Authors: Eosinophil Recruitment, Franco H Falcone, Xingxing Zang, Andrew S Macdonald, Rick M Maizels, During Nematode Infection, Judith E AllenAbstract:Infections with the helminth parasite Brugia malayi share many key features with Th2-mediated allergic diseases, including recruitment of Eosinophils. We have investigated the dynamics of inflammatory cell recruitment under type 2 cytokine conditions in mice infected with B. malayi. Among the cells recruited to the site of infection is a novel population of “alternatively activated” macrophages that ablate cell proliferation and enhance Th2 differentiation. By profiling gene expression in this macrophage population, we found a dramatic up-regulation of a recently described Eosinophil Chemotactic Factor, Eosinophil Chemotactic Factor-L/Ym1, representing over 9 % of clones randomly selected from a cDNA library. Because B. malayi is known to secrete homologs (Bm macrophage migration inhibitory Factor (MIF)-1 and-2) of the human cytokine MIF, we chose to investigate the role this cytokine mimic may play in the development of the novel macrophage phenotype observed during infection. Strikingly, administration of soluble recombinant Bm-MIF-1 was able to reproduce the effects of live parasites, leading both to the up-regulation of Ym1 by macrophages and a marked recruitment of Eosinophils in vivo. Because activity of Bm-MIF-1 is dependent upon an amino-terminal proline, this residue was mutated to glycine; the resultant recombinant (Bm-MIF-1G) was unable to induce Ym1 transcription in macrophages or to mediate the recruitment of Eosinophils. These data suggest that macrophages may provide a crucial link between helminth parasites, their active cytokine mimics, and the recruitment of Eosinophils in infection. The Journal of Immunology, 2001, 167: 5348–5354. I nfection with helminth parasites is associated with elevated IgE,systemic Eosinophilia, and mast cell proliferation (1). These fea-tures reflect a polarized type 2 T cell response enriched in IL-4
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a brugia malayi homolog of macrophage migration inhibitory Factor reveals an important link between macrophages and Eosinophil recruitment during nematode infection
Journal of Immunology, 2001Co-Authors: Franco H Falcone, Png Loke, Xingxing Zang, Andrew S Macdonald, Rick M Maizels, Judith E AllenAbstract:Infections with the helminth parasite Brugia malayi share many key features with Th2-mediated allergic diseases, including recruitment of Eosinophils. We have investigated the dynamics of inflammatory cell recruitment under type 2 cytokine conditions in mice infected with B. malayi. Among the cells recruited to the site of infection is a novel population of "alternatively activated" macrophages that ablate cell proliferation and enhance Th2 differentiation. By profiling gene expression in this macrophage population, we found a dramatic up-regulation of a recently described Eosinophil Chemotactic Factor, Eosinophil Chemotactic Factor-L/Ym1, representing over 9% of clones randomly selected from a cDNA library. Because B. malayi is known to secrete homologs (Bm macrophage migration inhibitory Factor (MIF)-1 and -2) of the human cytokine MIF, we chose to investigate the role this cytokine mimic may play in the development of the novel macrophage phenotype observed during infection. Strikingly, administration of soluble recombinant Bm-MIF-1 was able to reproduce the effects of live parasites, leading both to the up-regulation of Ym1 by macrophages and a marked recruitment of Eosinophils in vivo. Because activity of Bm-MIF-1 is dependent upon an amino-terminal proline, this residue was mutated to glycine; the resultant recombinant (Bm-MIF-1G) was unable to induce Ym1 transcription in macrophages or to mediate the recruitment of Eosinophils. These data suggest that macrophages may provide a crucial link between helminth parasites, their active cytokine mimics, and the recruitment of Eosinophils in infection.
David G Roodman - One of the best experts on this subject based on the ideXlab platform.
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Eosinophil Chemotactic Factor l ecf l enhances osteoclast formation by increasing in osteoclast precursors expression of lfa 1 and icam 1
Bone, 2007Co-Authors: Veronica Garciapalacios, Ho Yeon Chung, Sun Jin Choi, Noriyoshi Kurihara, Jun Won Lee, Robert L Collins, Aliye Sarmasik, Deborah L Galson, David G RoodmanAbstract:ECF-L is a novel autocrine stimulator of osteoclast (OCL) formation that enhances the effects of 1,25-(OH)2D3 and RANK ligand (RANKL) and is increased in inflammatory conditions such as rheumatoid arthritis. ECF-L acts at the later stages of OCL formation and does not increase RANKL expression. Thus, its mechanism of action is unclear. Therefore, RAW 264.7 cells and M-CSF-dependent murine bone marrow macrophage (MDBM) cells were treated with RANKL and/or with recombinant ECF-L expressed as a Fc fusion protein (ECF-L-Fc) to determine their effects on NF-kappaB, AP-1 and JNK activity, and on the expression of the adhesion molecules that have been implicated in OCL formation. These parameters were measured by semiquantitative and PCR and Western blot analysis. In addition, the role of ICAM-1 was further assessed by treating normal mouse marrow cultures with ECF-L-Fc and 10(-10) M 1,25-(OH)2D3 in the presence or absence of a blocking ICAM-1 antibody or treating marrow cultures from ICAM-1 knockout mice with ECF-L and 1,25-(OH)2D3. ECF-L-Fc by itself only modestly increased NF-kappaB binding and JNK activity in RAW 264.7 cells, which was further enhanced by RANKL. In contrast, ECF-L-Fc increased LFA-1alpha and ICAM-1 mRNA levels 1.8-fold in mouse marrow cultures, and anti-ICAM-1 almost completely inhibited OCL formation induced by 10(-10) M 1,25-(OH)2D3 and ECF-L. Furthermore, ECF-L did not increase OCL formation in marrow cultures from ICAM-1 knockout mice. Taken together, these results demonstrate that ECF-L enhances RANKL and 1,25-(OH)2D3-induced OCL formation by increasing adhesive interactions between OCL precursors through increased expression of ICAM-1 and LFA-1.
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Eosinophil Chemotactic Factor l ecf l enhances osteoclast formation by increasing icam 1 expression
Annals of the New York Academy of Sciences, 2006Co-Authors: Veronica Garcia Palacios, Ho Yeon Chung, Sun Jin Choi, Noriyoshi Kurihara, Jun Won Lee, Lori A Ehrlich, Robert L Collins, David G RoodmanAbstract:Eosinophil Chemotactic Factor-L (ECF-L) is a novel stimulator of osteoclast (OCL) formation that acts at the differentiation/fusion stage of OCL formation, and is a coFactor for RANK ligand (RANKL). We examined the effects of ECF-L on the intracellular signaling pathways utilized by RANKL, and on the expression of ICAM-1/LFA-1 to determine its mechanism of action. RAW 264.7 and bone marrow cells were treated with RANKL and/or ECF-L Fc protein to determine their effect on NF-kappaB and AP-1 activity. ECF-L by itself only modestly increased NF-kappaB binding and JNK activity in RAW 264.7 cells, which were further enhanced by RANKL. In contrast, ECF-L Fc increased LFA-1alpha and ICAM-1 mRNA levels 1.8-fold in mouse marrow cultures, and anti-ICAM-1 almost completely inhibited OCL formation induced by 10(-10) M 1,25-(OH)2D3, and ECF-L Fc. Furthermore, ECF-L Fc did not enhance OCL formation by ICAM-1 knockout (KO) cells. Increased expression of ICAM-1 by ECF-L appears to be critical for its effects on OCL formation.
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regulation of osteoclast differentiation
Annals of the New York Academy of Sciences, 2006Co-Authors: David G RoodmanAbstract:The osteoclast (OCL) is derived from the cells in monocyte- macrophage lineage. The earliest identifiable OCL precursor is the granulocyte-macrophage colony-forming unit (CFU-GM), which gives rise to granulocytes, monocytes, and OCL. CFU-GM-derived cells then differentiate to committed OCL precursors, which are post-mitotic cells, and fuse to form multinucleated OCL. A variety of Factors both posi- tively and negatively regulate OCL formation and activity. These include growth Factors, such as macrophage colony-simulating Factor, which sim- ulates the proliferation and prevents apoptosis of early OCL precursors, and RANK ligand (RANKL), which is the primary mediator of OCL for- mation. Most Factors that induce OCL differentiation, such as PTHrP, IL-11, and prostaglandins, do so by inducing expression of RANKL on the surface of immature osteoblasts. Osteoprotegerin is a decoy recep- tor that blocks RANKL activity. In addition, OCL produce autocrine- paracrine Factors that regulate OCL formation, such as IL-6, which is produced at high levels by OCL in Paget's disease and increases OCL formation. We screened human and murine OCL cDNA libraries to iden- tify autocrine-paracrine Factors that regulate OCL activity. We identified annexin-II, MIP-1� , ADAM8, Eosinophil Chemotactic Factor, and OCL inhibitor Factors 1 and 2 as Factors involved in OCL formation. Most re- cently, we have identified the receptor for ADAM8, � 9� 1 integrin, which appears to be critical for normal OCL activity. OCL differentiation is controlled by exogenous hormones and cytokines as well as autocrine- paracrine Factors that positively or negatively regulate OCL proliferation and differentiation.
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Eosinophil Chemotactic Factor l ecf l a novel osteoclast stimulating Factor
Journal of Bone and Mineral Research, 2003Co-Authors: Yasuo Oba, Ho Yeon Chung, Sun Jin Choi, David G RoodmanAbstract:Screening a cDNA library enriched for genes expressed in OCLs identified ECF-L. ECF-L enhanced OCL formation without increasing RANKL levels. Anti-ECF-L inhibited RANKL-induced OCL formation. These results support a potent role of ECF-L in osteoclastogenesis. Introduction: To investigate the molecular mechanisms that control osteoclastogenesis, we developed an immortalized osteoclast (OCL) precursor cell line that forms mature OCLs in the absence of stromal cells and used it to form pure populations of OCLs. Materials and Methods: Polymerase chain reaction (PCR) selective cDNA subtraction was used to identify genes that are highly expressed in mature OCLs compared with OCL precursors employing OCL and OCL precursors derived from this cell line. Results: Eosinophil Chemotactic Factor-L (ECF-L), a previously described Chemotactic Factor for Eosinophils, was one of the genes identified. Conditioned media from 293 cells transfected with mECF-L cDNA, or purified ECF-L Fc protein, increased OCL formation in a dose-dependent manner in mouse bone marrow cultures treated with 10−10 M 1,25(OH)2D3. OCLs derived from marrow cultures treated with ECF-L conditioned media formed increased pit numbers and resorption area per dentin slice compared with OCLs induced by 1,25(OH)2D3 (p < 0.01). Addition of an antisense S-oligonucleotide to mECF-L inhibited OCL formation in murine bone marrow cultures treated only with 10−9 M 1,25(OH)2D3 compared with the sense S-oligonucleotide control. Time course studies demonstrated that ECF-L acted at the later stages of OCL formation, and Chemotactic assays showed that mECF-L increased migration of OCL precursors. mECF-L mRNA was detectable in mononuclear and multinucleated cells by in situ hybridization. Interestingly, a neutralizing antibody to ECF-L blocked RANKL or 10−9 M 1,25(OH)2D3-induced OCL formation in mouse bone marrow cultures, although ECF-L did not induce RANKL expression. Conclusions: These data show ECF-L is a previously unknown Factor that is a potent mediator of OCL formation, which acts at the later stages of OCL formation and enhances the effects of RANKL.
Franco H Falcone - One of the best experts on this subject based on the ideXlab platform.
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A Brugia malayi Homolog of Macrophage Migration Inhibitory Factor Reveals an Important Link Between Macrophages and
2014Co-Authors: Eosinophil Recruitment, Franco H Falcone, Xingxing Zang, Andrew S Macdonald, Rick M Maizels, During Nematode Infection, Judith E AllenAbstract:Infections with the helminth parasite Brugia malayi share many key features with Th2-mediated allergic diseases, including recruitment of Eosinophils. We have investigated the dynamics of inflammatory cell recruitment under type 2 cytokine conditions in mice infected with B. malayi. Among the cells recruited to the site of infection is a novel population of “alternatively activated” macrophages that ablate cell proliferation and enhance Th2 differentiation. By profiling gene expression in this macrophage population, we found a dramatic up-regulation of a recently described Eosinophil Chemotactic Factor, Eosinophil Chemotactic Factor-L/Ym1, representing over 9 % of clones randomly selected from a cDNA library. Because B. malayi is known to secrete homologs (Bm macrophage migration inhibitory Factor (MIF)-1 and-2) of the human cytokine MIF, we chose to investigate the role this cytokine mimic may play in the development of the novel macrophage phenotype observed during infection. Strikingly, administration of soluble recombinant Bm-MIF-1 was able to reproduce the effects of live parasites, leading both to the up-regulation of Ym1 by macrophages and a marked recruitment of Eosinophils in vivo. Because activity of Bm-MIF-1 is dependent upon an amino-terminal proline, this residue was mutated to glycine; the resultant recombinant (Bm-MIF-1G) was unable to induce Ym1 transcription in macrophages or to mediate the recruitment of Eosinophils. These data suggest that macrophages may provide a crucial link between helminth parasites, their active cytokine mimics, and the recruitment of Eosinophils in infection. The Journal of Immunology, 2001, 167: 5348–5354. I nfection with helminth parasites is associated with elevated IgE,systemic Eosinophilia, and mast cell proliferation (1). These fea-tures reflect a polarized type 2 T cell response enriched in IL-4
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a brugia malayi homolog of macrophage migration inhibitory Factor reveals an important link between macrophages and Eosinophil recruitment during nematode infection
Journal of Immunology, 2001Co-Authors: Franco H Falcone, Png Loke, Xingxing Zang, Andrew S Macdonald, Rick M Maizels, Judith E AllenAbstract:Infections with the helminth parasite Brugia malayi share many key features with Th2-mediated allergic diseases, including recruitment of Eosinophils. We have investigated the dynamics of inflammatory cell recruitment under type 2 cytokine conditions in mice infected with B. malayi. Among the cells recruited to the site of infection is a novel population of "alternatively activated" macrophages that ablate cell proliferation and enhance Th2 differentiation. By profiling gene expression in this macrophage population, we found a dramatic up-regulation of a recently described Eosinophil Chemotactic Factor, Eosinophil Chemotactic Factor-L/Ym1, representing over 9% of clones randomly selected from a cDNA library. Because B. malayi is known to secrete homologs (Bm macrophage migration inhibitory Factor (MIF)-1 and -2) of the human cytokine MIF, we chose to investigate the role this cytokine mimic may play in the development of the novel macrophage phenotype observed during infection. Strikingly, administration of soluble recombinant Bm-MIF-1 was able to reproduce the effects of live parasites, leading both to the up-regulation of Ym1 by macrophages and a marked recruitment of Eosinophils in vivo. Because activity of Bm-MIF-1 is dependent upon an amino-terminal proline, this residue was mutated to glycine; the resultant recombinant (Bm-MIF-1G) was unable to induce Ym1 transcription in macrophages or to mediate the recruitment of Eosinophils. These data suggest that macrophages may provide a crucial link between helminth parasites, their active cytokine mimics, and the recruitment of Eosinophils in infection.