A nuclear factor-κB inhibitor, dehydroxymethylepoxyquinomicin, ameliorates GVHD in allogeneic bone marrow transplantation
GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57B...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Yamanouchi, Sohsaku [verfasserIn] |
|---|
| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015transfer abstract |
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| Schlagwörter: |
Allogeneic bone marrow transplantation |
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| Umfang: |
8 |
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| Übergeordnetes Werk: |
Enthalten in: Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center - Clark, Leon G. ELSEVIER, 2016, experimental and clinical, München |
|---|---|
| Übergeordnetes Werk: |
volume:220 ; year:2015 ; number:9 ; pages:1059-1066 ; extent:8 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.imbio.2015.05.011 |
|---|
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ELV039668479 |
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| 245 | 1 | 0 | |a A nuclear factor-κB inhibitor, dehydroxymethylepoxyquinomicin, ameliorates GVHD in allogeneic bone marrow transplantation |
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| 520 | |a GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. | ||
| 520 | |a GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. | ||
| 650 | 7 | |a NF-κB |2 Elsevier | |
| 650 | 7 | |a Graft versus host disease |2 Elsevier | |
| 650 | 7 | |a Allogeneic bone marrow transplantation |2 Elsevier | |
| 650 | 7 | |a Regulatory T cell |2 Elsevier | |
| 650 | 7 | |a Dehydroxymethylepoxyquinomicin (DHMEQ) |2 Elsevier | |
| 650 | 7 | |a Survival rate |2 Elsevier | |
| 700 | 1 | |a Adachi, Yasushi |4 oth | |
| 700 | 1 | |a Shimo, Tomohiko |4 oth | |
| 700 | 1 | |a Umezawa, Kazuo |4 oth | |
| 700 | 1 | |a Okigaki, Mitsuhiko |4 oth | |
| 700 | 1 | |a Tsuji, Shoji |4 oth | |
| 700 | 1 | |a Li, Ming |4 oth | |
| 700 | 1 | |a Takaya, Junji |4 oth | |
| 700 | 1 | |a Kuge, Tomohiro |4 oth | |
| 700 | 1 | |a Ikehara, Susumu |4 oth | |
| 700 | 1 | |a Kaneko, Kazunari |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier |a Clark, Leon G. ELSEVIER |t Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center |d 2016 |d experimental and clinical |g München |w (DE-627)ELV013869728 |
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10.1016/j.imbio.2015.05.011 doi GBVA2015006000023.pica (DE-627)ELV039668479 (ELSEVIER)S0171-2985(15)00079-0 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Yamanouchi, Sohsaku verfasserin aut A nuclear factor-κB inhibitor, dehydroxymethylepoxyquinomicin, ameliorates GVHD in allogeneic bone marrow transplantation 2015transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. NF-κB Elsevier Graft versus host disease Elsevier Allogeneic bone marrow transplantation Elsevier Regulatory T cell Elsevier Dehydroxymethylepoxyquinomicin (DHMEQ) Elsevier Survival rate Elsevier Adachi, Yasushi oth Shimo, Tomohiko oth Umezawa, Kazuo oth Okigaki, Mitsuhiko oth Tsuji, Shoji oth Li, Ming oth Takaya, Junji oth Kuge, Tomohiro oth Ikehara, Susumu oth Kaneko, Kazunari oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:220 year:2015 number:9 pages:1059-1066 extent:8 https://doi.org/10.1016/j.imbio.2015.05.011 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 220 2015 9 1059-1066 8 045F 570 |
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10.1016/j.imbio.2015.05.011 doi GBVA2015006000023.pica (DE-627)ELV039668479 (ELSEVIER)S0171-2985(15)00079-0 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Yamanouchi, Sohsaku verfasserin aut A nuclear factor-κB inhibitor, dehydroxymethylepoxyquinomicin, ameliorates GVHD in allogeneic bone marrow transplantation 2015transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. NF-κB Elsevier Graft versus host disease Elsevier Allogeneic bone marrow transplantation Elsevier Regulatory T cell Elsevier Dehydroxymethylepoxyquinomicin (DHMEQ) Elsevier Survival rate Elsevier Adachi, Yasushi oth Shimo, Tomohiko oth Umezawa, Kazuo oth Okigaki, Mitsuhiko oth Tsuji, Shoji oth Li, Ming oth Takaya, Junji oth Kuge, Tomohiro oth Ikehara, Susumu oth Kaneko, Kazunari oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:220 year:2015 number:9 pages:1059-1066 extent:8 https://doi.org/10.1016/j.imbio.2015.05.011 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 220 2015 9 1059-1066 8 045F 570 |
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10.1016/j.imbio.2015.05.011 doi GBVA2015006000023.pica (DE-627)ELV039668479 (ELSEVIER)S0171-2985(15)00079-0 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Yamanouchi, Sohsaku verfasserin aut A nuclear factor-κB inhibitor, dehydroxymethylepoxyquinomicin, ameliorates GVHD in allogeneic bone marrow transplantation 2015transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. NF-κB Elsevier Graft versus host disease Elsevier Allogeneic bone marrow transplantation Elsevier Regulatory T cell Elsevier Dehydroxymethylepoxyquinomicin (DHMEQ) Elsevier Survival rate Elsevier Adachi, Yasushi oth Shimo, Tomohiko oth Umezawa, Kazuo oth Okigaki, Mitsuhiko oth Tsuji, Shoji oth Li, Ming oth Takaya, Junji oth Kuge, Tomohiro oth Ikehara, Susumu oth Kaneko, Kazunari oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:220 year:2015 number:9 pages:1059-1066 extent:8 https://doi.org/10.1016/j.imbio.2015.05.011 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 220 2015 9 1059-1066 8 045F 570 |
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10.1016/j.imbio.2015.05.011 doi GBVA2015006000023.pica (DE-627)ELV039668479 (ELSEVIER)S0171-2985(15)00079-0 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Yamanouchi, Sohsaku verfasserin aut A nuclear factor-κB inhibitor, dehydroxymethylepoxyquinomicin, ameliorates GVHD in allogeneic bone marrow transplantation 2015transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. NF-κB Elsevier Graft versus host disease Elsevier Allogeneic bone marrow transplantation Elsevier Regulatory T cell Elsevier Dehydroxymethylepoxyquinomicin (DHMEQ) Elsevier Survival rate Elsevier Adachi, Yasushi oth Shimo, Tomohiko oth Umezawa, Kazuo oth Okigaki, Mitsuhiko oth Tsuji, Shoji oth Li, Ming oth Takaya, Junji oth Kuge, Tomohiro oth Ikehara, Susumu oth Kaneko, Kazunari oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:220 year:2015 number:9 pages:1059-1066 extent:8 https://doi.org/10.1016/j.imbio.2015.05.011 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 220 2015 9 1059-1066 8 045F 570 |
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10.1016/j.imbio.2015.05.011 doi GBVA2015006000023.pica (DE-627)ELV039668479 (ELSEVIER)S0171-2985(15)00079-0 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Yamanouchi, Sohsaku verfasserin aut A nuclear factor-κB inhibitor, dehydroxymethylepoxyquinomicin, ameliorates GVHD in allogeneic bone marrow transplantation 2015transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. NF-κB Elsevier Graft versus host disease Elsevier Allogeneic bone marrow transplantation Elsevier Regulatory T cell Elsevier Dehydroxymethylepoxyquinomicin (DHMEQ) Elsevier Survival rate Elsevier Adachi, Yasushi oth Shimo, Tomohiko oth Umezawa, Kazuo oth Okigaki, Mitsuhiko oth Tsuji, Shoji oth Li, Ming oth Takaya, Junji oth Kuge, Tomohiro oth Ikehara, Susumu oth Kaneko, Kazunari oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:220 year:2015 number:9 pages:1059-1066 extent:8 https://doi.org/10.1016/j.imbio.2015.05.011 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 220 2015 9 1059-1066 8 045F 570 |
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Enthalten in Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center München volume:220 year:2015 number:9 pages:1059-1066 extent:8 |
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A nuclear factor-κB inhibitor, dehydroxymethylepoxyquinomicin, ameliorates GVHD in allogeneic bone marrow transplantation |
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GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. |
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GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. |
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GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD. |
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These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">GVHD is a crucial mortality factor in allogeneic bone marrow transplantation (ABMT). In this paper, we show that dehydroxymethylepoxyquinomicin (DHMEQ), a novel inhibitor of nuclear factor-κB, suppresses GVHD, resulting in an improved mortality rate in a mouse ABMT model. Bone marrow cells from C57BL/6 mice (B6 mice) were transplanted into lethally irradiated BALB/c mice. Two weeks later, spleen cells from B6 mice were transplanted into the irradiated BALB/c mice. From one week after the injection of spleen cells, when the mice started to show GVHD, the mice were also injected intraperitoneally daily with DHMEQ or vehicle only (DMSO) for 4 weeks. By 80 days after the ABMT, 6/14 of the vehicle-injected mice (43%) had died because of GVHD, whereas all DHMEQ-injected mice survived this observation period and developed milder GVHD than the vehicle-injected mice. When regulatory T cells were reduced by the injection of anti-folate receptor 4 (FR4) antibody, the effects of DHMEQ were reduced. These findings suggest that administration of DHMEQ could become a new strategy for preventing fatalities from GVHD.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NF-κB</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Graft versus host disease</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Allogeneic bone marrow transplantation</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Regulatory T cell</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Dehydroxymethylepoxyquinomicin (DHMEQ)</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Survival rate</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Adachi, Yasushi</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Shimo, Tomohiko</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Umezawa, Kazuo</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Okigaki, Mitsuhiko</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Tsuji, Shoji</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Ming</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Takaya, Junji</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kuge, Tomohiro</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ikehara, Susumu</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kaneko, Kazunari</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Clark, Leon G. ELSEVIER</subfield><subfield code="t">Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center</subfield><subfield code="d">2016</subfield><subfield code="d">experimental and clinical</subfield><subfield code="g">München</subfield><subfield code="w">(DE-627)ELV013869728</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:220</subfield><subfield code="g">year:2015</subfield><subfield code="g">number:9</subfield><subfield code="g">pages:1059-1066</subfield><subfield code="g">extent:8</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.imbio.2015.05.011</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-GGO</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">43.12</subfield><subfield code="j">Umweltchemie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">43.13</subfield><subfield code="j">Umwelttoxikologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.13</subfield><subfield code="j">Medizinische Ökologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">220</subfield><subfield code="j">2015</subfield><subfield code="e">9</subfield><subfield code="h">1059-1066</subfield><subfield code="g">8</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">570</subfield></datafield></record></collection>
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