Intracellular Calcium Affects Neutrophil Chemoattractant Expression by Macrophages in Rats with Cerulein-Induced Pancreatitis
Abstract Pancreatitis complicated with infection oftenresults in the development of multiple organ failure. Weinvestigated the role of altered intracellular calciumas a priming signal for cytokine-induced neutrophil chemoattractant expression in this process.Agents modulating cytosolic Ca2+ wereutil...
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1998 |
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| Umfang: |
7 |
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| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Digestive diseases and sciences - 1956, 43(1998) vom: Apr., Seite 863-869 |
| Übergeordnetes Werk: |
volume:43 ; year:1998 ; month:04 ; pages:863-869 ; extent:7 |
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NLEJ197046347 |
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| 520 | |a Abstract Pancreatitis complicated with infection oftenresults in the development of multiple organ failure. Weinvestigated the role of altered intracellular calciumas a priming signal for cytokine-induced neutrophil chemoattractant expression in this process.Agents modulating cytosolic Ca2+ wereutilized to study the in vivo and in vitrocytokine-induced neutrophil chemoattractant expressionfor macrophages in rats with cerulein-induced pancreatitis afterintraperitoneal administration of lipopolysaccharide asa septic challenge. Pretreatment with the calciumchannel blocker verapamil significantly reduced serumcytokine-induced neutrophil chemoattractant concentrations inrats with cerulein-induced pancreatitis after septicchallenge. Lipopolysaccharide-stimulated in vitrocytokine-induced neutrophil chemoattractant (CINC)production by peritoneal macrophages was significantlyenhanced by pretreatment with thapsigargin (an inhibitorof the endoplasmic reticulum-resident Ca2+-ATPase), but not by A23187 (acalcium-specific ionophore, extracellular Ca2+ influx). Pretreatment withU73122 (a phospholipase C inhibitor) inhibitedlipopolysaccharide-stimulated but not basalcytokine-induced neutrophil chemoattractant production,while verapamil (a calcium channel blocker), TMB-8 (an inhibitor ofcalcium release from endoplasmic reticulum), and W7(calmodulin antagonist) completely abrogated thechemoattractant production. Altered intracellularcalcium, due to Ca2+ efflux from intracellularstores, may be involved in the “priming” ofmacrophages to release cytokine-induced neutrophilchemoattractant following triggering withlipopolysaccharide during acute cerulein pancreatitis. | ||
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| 700 | 1 | |a Akizuki, Eiji |4 oth | |
| 700 | 1 | |a Matsumura, Fujio |4 oth | |
| 700 | 1 | |a Okabe, Kazutoshi |4 oth | |
| 700 | 1 | |a Liang, Jian |4 oth | |
| 700 | 1 | |a Matsuda, Teishi |4 oth | |
| 700 | 1 | |a Yamada, Shinwa |4 oth | |
| 700 | 1 | |a Ogawa, Michio |4 oth | |
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(DE-627)NLEJ197046347 DE-627 ger DE-627 rakwb eng Intracellular Calcium Affects Neutrophil Chemoattractant Expression by Macrophages in Rats with Cerulein-Induced Pancreatitis 1998 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Pancreatitis complicated with infection oftenresults in the development of multiple organ failure. Weinvestigated the role of altered intracellular calciumas a priming signal for cytokine-induced neutrophil chemoattractant expression in this process.Agents modulating cytosolic Ca2+ wereutilized to study the in vivo and in vitrocytokine-induced neutrophil chemoattractant expressionfor macrophages in rats with cerulein-induced pancreatitis afterintraperitoneal administration of lipopolysaccharide asa septic challenge. Pretreatment with the calciumchannel blocker verapamil significantly reduced serumcytokine-induced neutrophil chemoattractant concentrations inrats with cerulein-induced pancreatitis after septicchallenge. Lipopolysaccharide-stimulated in vitrocytokine-induced neutrophil chemoattractant (CINC)production by peritoneal macrophages was significantlyenhanced by pretreatment with thapsigargin (an inhibitorof the endoplasmic reticulum-resident Ca2+-ATPase), but not by A23187 (acalcium-specific ionophore, extracellular Ca2+ influx). Pretreatment withU73122 (a phospholipase C inhibitor) inhibitedlipopolysaccharide-stimulated but not basalcytokine-induced neutrophil chemoattractant production,while verapamil (a calcium channel blocker), TMB-8 (an inhibitor ofcalcium release from endoplasmic reticulum), and W7(calmodulin antagonist) completely abrogated thechemoattractant production. Altered intracellularcalcium, due to Ca2+ efflux from intracellularstores, may be involved in the “priming” ofmacrophages to release cytokine-induced neutrophilchemoattractant following triggering withlipopolysaccharide during acute cerulein pancreatitis. Springer Online Journal Archives 1860-2002 Yamaguchi, Yasuo oth Akizuki, Eiji oth Matsumura, Fujio oth Okabe, Kazutoshi oth Liang, Jian oth Matsuda, Teishi oth Yamada, Shinwa oth Ogawa, Michio oth in Digestive diseases and sciences 1956 43(1998) vom: Apr., Seite 863-869 (DE-627)NLEJ18898948X (DE-600)2015102-0 1573-2568 nnns volume:43 year:1998 month:04 pages:863-869 extent:7 http://dx.doi.org/10.1023/A:1018890703661 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 43 1998 4 863-869 7 |
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(DE-627)NLEJ197046347 DE-627 ger DE-627 rakwb eng Intracellular Calcium Affects Neutrophil Chemoattractant Expression by Macrophages in Rats with Cerulein-Induced Pancreatitis 1998 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Pancreatitis complicated with infection oftenresults in the development of multiple organ failure. Weinvestigated the role of altered intracellular calciumas a priming signal for cytokine-induced neutrophil chemoattractant expression in this process.Agents modulating cytosolic Ca2+ wereutilized to study the in vivo and in vitrocytokine-induced neutrophil chemoattractant expressionfor macrophages in rats with cerulein-induced pancreatitis afterintraperitoneal administration of lipopolysaccharide asa septic challenge. Pretreatment with the calciumchannel blocker verapamil significantly reduced serumcytokine-induced neutrophil chemoattractant concentrations inrats with cerulein-induced pancreatitis after septicchallenge. Lipopolysaccharide-stimulated in vitrocytokine-induced neutrophil chemoattractant (CINC)production by peritoneal macrophages was significantlyenhanced by pretreatment with thapsigargin (an inhibitorof the endoplasmic reticulum-resident Ca2+-ATPase), but not by A23187 (acalcium-specific ionophore, extracellular Ca2+ influx). Pretreatment withU73122 (a phospholipase C inhibitor) inhibitedlipopolysaccharide-stimulated but not basalcytokine-induced neutrophil chemoattractant production,while verapamil (a calcium channel blocker), TMB-8 (an inhibitor ofcalcium release from endoplasmic reticulum), and W7(calmodulin antagonist) completely abrogated thechemoattractant production. Altered intracellularcalcium, due to Ca2+ efflux from intracellularstores, may be involved in the “priming” ofmacrophages to release cytokine-induced neutrophilchemoattractant following triggering withlipopolysaccharide during acute cerulein pancreatitis. Springer Online Journal Archives 1860-2002 Yamaguchi, Yasuo oth Akizuki, Eiji oth Matsumura, Fujio oth Okabe, Kazutoshi oth Liang, Jian oth Matsuda, Teishi oth Yamada, Shinwa oth Ogawa, Michio oth in Digestive diseases and sciences 1956 43(1998) vom: Apr., Seite 863-869 (DE-627)NLEJ18898948X (DE-600)2015102-0 1573-2568 nnns volume:43 year:1998 month:04 pages:863-869 extent:7 http://dx.doi.org/10.1023/A:1018890703661 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 43 1998 4 863-869 7 |
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(DE-627)NLEJ197046347 DE-627 ger DE-627 rakwb eng Intracellular Calcium Affects Neutrophil Chemoattractant Expression by Macrophages in Rats with Cerulein-Induced Pancreatitis 1998 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Pancreatitis complicated with infection oftenresults in the development of multiple organ failure. Weinvestigated the role of altered intracellular calciumas a priming signal for cytokine-induced neutrophil chemoattractant expression in this process.Agents modulating cytosolic Ca2+ wereutilized to study the in vivo and in vitrocytokine-induced neutrophil chemoattractant expressionfor macrophages in rats with cerulein-induced pancreatitis afterintraperitoneal administration of lipopolysaccharide asa septic challenge. Pretreatment with the calciumchannel blocker verapamil significantly reduced serumcytokine-induced neutrophil chemoattractant concentrations inrats with cerulein-induced pancreatitis after septicchallenge. Lipopolysaccharide-stimulated in vitrocytokine-induced neutrophil chemoattractant (CINC)production by peritoneal macrophages was significantlyenhanced by pretreatment with thapsigargin (an inhibitorof the endoplasmic reticulum-resident Ca2+-ATPase), but not by A23187 (acalcium-specific ionophore, extracellular Ca2+ influx). Pretreatment withU73122 (a phospholipase C inhibitor) inhibitedlipopolysaccharide-stimulated but not basalcytokine-induced neutrophil chemoattractant production,while verapamil (a calcium channel blocker), TMB-8 (an inhibitor ofcalcium release from endoplasmic reticulum), and W7(calmodulin antagonist) completely abrogated thechemoattractant production. Altered intracellularcalcium, due to Ca2+ efflux from intracellularstores, may be involved in the “priming” ofmacrophages to release cytokine-induced neutrophilchemoattractant following triggering withlipopolysaccharide during acute cerulein pancreatitis. Springer Online Journal Archives 1860-2002 Yamaguchi, Yasuo oth Akizuki, Eiji oth Matsumura, Fujio oth Okabe, Kazutoshi oth Liang, Jian oth Matsuda, Teishi oth Yamada, Shinwa oth Ogawa, Michio oth in Digestive diseases and sciences 1956 43(1998) vom: Apr., Seite 863-869 (DE-627)NLEJ18898948X (DE-600)2015102-0 1573-2568 nnns volume:43 year:1998 month:04 pages:863-869 extent:7 http://dx.doi.org/10.1023/A:1018890703661 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 43 1998 4 863-869 7 |
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(DE-627)NLEJ197046347 DE-627 ger DE-627 rakwb eng Intracellular Calcium Affects Neutrophil Chemoattractant Expression by Macrophages in Rats with Cerulein-Induced Pancreatitis 1998 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Pancreatitis complicated with infection oftenresults in the development of multiple organ failure. Weinvestigated the role of altered intracellular calciumas a priming signal for cytokine-induced neutrophil chemoattractant expression in this process.Agents modulating cytosolic Ca2+ wereutilized to study the in vivo and in vitrocytokine-induced neutrophil chemoattractant expressionfor macrophages in rats with cerulein-induced pancreatitis afterintraperitoneal administration of lipopolysaccharide asa septic challenge. Pretreatment with the calciumchannel blocker verapamil significantly reduced serumcytokine-induced neutrophil chemoattractant concentrations inrats with cerulein-induced pancreatitis after septicchallenge. Lipopolysaccharide-stimulated in vitrocytokine-induced neutrophil chemoattractant (CINC)production by peritoneal macrophages was significantlyenhanced by pretreatment with thapsigargin (an inhibitorof the endoplasmic reticulum-resident Ca2+-ATPase), but not by A23187 (acalcium-specific ionophore, extracellular Ca2+ influx). Pretreatment withU73122 (a phospholipase C inhibitor) inhibitedlipopolysaccharide-stimulated but not basalcytokine-induced neutrophil chemoattractant production,while verapamil (a calcium channel blocker), TMB-8 (an inhibitor ofcalcium release from endoplasmic reticulum), and W7(calmodulin antagonist) completely abrogated thechemoattractant production. Altered intracellularcalcium, due to Ca2+ efflux from intracellularstores, may be involved in the “priming” ofmacrophages to release cytokine-induced neutrophilchemoattractant following triggering withlipopolysaccharide during acute cerulein pancreatitis. Springer Online Journal Archives 1860-2002 Yamaguchi, Yasuo oth Akizuki, Eiji oth Matsumura, Fujio oth Okabe, Kazutoshi oth Liang, Jian oth Matsuda, Teishi oth Yamada, Shinwa oth Ogawa, Michio oth in Digestive diseases and sciences 1956 43(1998) vom: Apr., Seite 863-869 (DE-627)NLEJ18898948X (DE-600)2015102-0 1573-2568 nnns volume:43 year:1998 month:04 pages:863-869 extent:7 http://dx.doi.org/10.1023/A:1018890703661 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 43 1998 4 863-869 7 |
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(DE-627)NLEJ197046347 DE-627 ger DE-627 rakwb eng Intracellular Calcium Affects Neutrophil Chemoattractant Expression by Macrophages in Rats with Cerulein-Induced Pancreatitis 1998 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Pancreatitis complicated with infection oftenresults in the development of multiple organ failure. Weinvestigated the role of altered intracellular calciumas a priming signal for cytokine-induced neutrophil chemoattractant expression in this process.Agents modulating cytosolic Ca2+ wereutilized to study the in vivo and in vitrocytokine-induced neutrophil chemoattractant expressionfor macrophages in rats with cerulein-induced pancreatitis afterintraperitoneal administration of lipopolysaccharide asa septic challenge. Pretreatment with the calciumchannel blocker verapamil significantly reduced serumcytokine-induced neutrophil chemoattractant concentrations inrats with cerulein-induced pancreatitis after septicchallenge. Lipopolysaccharide-stimulated in vitrocytokine-induced neutrophil chemoattractant (CINC)production by peritoneal macrophages was significantlyenhanced by pretreatment with thapsigargin (an inhibitorof the endoplasmic reticulum-resident Ca2+-ATPase), but not by A23187 (acalcium-specific ionophore, extracellular Ca2+ influx). Pretreatment withU73122 (a phospholipase C inhibitor) inhibitedlipopolysaccharide-stimulated but not basalcytokine-induced neutrophil chemoattractant production,while verapamil (a calcium channel blocker), TMB-8 (an inhibitor ofcalcium release from endoplasmic reticulum), and W7(calmodulin antagonist) completely abrogated thechemoattractant production. Altered intracellularcalcium, due to Ca2+ efflux from intracellularstores, may be involved in the “priming” ofmacrophages to release cytokine-induced neutrophilchemoattractant following triggering withlipopolysaccharide during acute cerulein pancreatitis. Springer Online Journal Archives 1860-2002 Yamaguchi, Yasuo oth Akizuki, Eiji oth Matsumura, Fujio oth Okabe, Kazutoshi oth Liang, Jian oth Matsuda, Teishi oth Yamada, Shinwa oth Ogawa, Michio oth in Digestive diseases and sciences 1956 43(1998) vom: Apr., Seite 863-869 (DE-627)NLEJ18898948X (DE-600)2015102-0 1573-2568 nnns volume:43 year:1998 month:04 pages:863-869 extent:7 http://dx.doi.org/10.1023/A:1018890703661 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 43 1998 4 863-869 7 |
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intracellular calcium affects neutrophil chemoattractant expression by macrophages in rats with cerulein-induced pancreatitis |
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Intracellular Calcium Affects Neutrophil Chemoattractant Expression by Macrophages in Rats with Cerulein-Induced Pancreatitis |
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Abstract Pancreatitis complicated with infection oftenresults in the development of multiple organ failure. Weinvestigated the role of altered intracellular calciumas a priming signal for cytokine-induced neutrophil chemoattractant expression in this process.Agents modulating cytosolic Ca2+ wereutilized to study the in vivo and in vitrocytokine-induced neutrophil chemoattractant expressionfor macrophages in rats with cerulein-induced pancreatitis afterintraperitoneal administration of lipopolysaccharide asa septic challenge. Pretreatment with the calciumchannel blocker verapamil significantly reduced serumcytokine-induced neutrophil chemoattractant concentrations inrats with cerulein-induced pancreatitis after septicchallenge. Lipopolysaccharide-stimulated in vitrocytokine-induced neutrophil chemoattractant (CINC)production by peritoneal macrophages was significantlyenhanced by pretreatment with thapsigargin (an inhibitorof the endoplasmic reticulum-resident Ca2+-ATPase), but not by A23187 (acalcium-specific ionophore, extracellular Ca2+ influx). Pretreatment withU73122 (a phospholipase C inhibitor) inhibitedlipopolysaccharide-stimulated but not basalcytokine-induced neutrophil chemoattractant production,while verapamil (a calcium channel blocker), TMB-8 (an inhibitor ofcalcium release from endoplasmic reticulum), and W7(calmodulin antagonist) completely abrogated thechemoattractant production. Altered intracellularcalcium, due to Ca2+ efflux from intracellularstores, may be involved in the “priming” ofmacrophages to release cytokine-induced neutrophilchemoattractant following triggering withlipopolysaccharide during acute cerulein pancreatitis. |
| abstractGer |
Abstract Pancreatitis complicated with infection oftenresults in the development of multiple organ failure. Weinvestigated the role of altered intracellular calciumas a priming signal for cytokine-induced neutrophil chemoattractant expression in this process.Agents modulating cytosolic Ca2+ wereutilized to study the in vivo and in vitrocytokine-induced neutrophil chemoattractant expressionfor macrophages in rats with cerulein-induced pancreatitis afterintraperitoneal administration of lipopolysaccharide asa septic challenge. Pretreatment with the calciumchannel blocker verapamil significantly reduced serumcytokine-induced neutrophil chemoattractant concentrations inrats with cerulein-induced pancreatitis after septicchallenge. Lipopolysaccharide-stimulated in vitrocytokine-induced neutrophil chemoattractant (CINC)production by peritoneal macrophages was significantlyenhanced by pretreatment with thapsigargin (an inhibitorof the endoplasmic reticulum-resident Ca2+-ATPase), but not by A23187 (acalcium-specific ionophore, extracellular Ca2+ influx). Pretreatment withU73122 (a phospholipase C inhibitor) inhibitedlipopolysaccharide-stimulated but not basalcytokine-induced neutrophil chemoattractant production,while verapamil (a calcium channel blocker), TMB-8 (an inhibitor ofcalcium release from endoplasmic reticulum), and W7(calmodulin antagonist) completely abrogated thechemoattractant production. Altered intracellularcalcium, due to Ca2+ efflux from intracellularstores, may be involved in the “priming” ofmacrophages to release cytokine-induced neutrophilchemoattractant following triggering withlipopolysaccharide during acute cerulein pancreatitis. |
| abstract_unstemmed |
Abstract Pancreatitis complicated with infection oftenresults in the development of multiple organ failure. Weinvestigated the role of altered intracellular calciumas a priming signal for cytokine-induced neutrophil chemoattractant expression in this process.Agents modulating cytosolic Ca2+ wereutilized to study the in vivo and in vitrocytokine-induced neutrophil chemoattractant expressionfor macrophages in rats with cerulein-induced pancreatitis afterintraperitoneal administration of lipopolysaccharide asa septic challenge. Pretreatment with the calciumchannel blocker verapamil significantly reduced serumcytokine-induced neutrophil chemoattractant concentrations inrats with cerulein-induced pancreatitis after septicchallenge. Lipopolysaccharide-stimulated in vitrocytokine-induced neutrophil chemoattractant (CINC)production by peritoneal macrophages was significantlyenhanced by pretreatment with thapsigargin (an inhibitorof the endoplasmic reticulum-resident Ca2+-ATPase), but not by A23187 (acalcium-specific ionophore, extracellular Ca2+ influx). Pretreatment withU73122 (a phospholipase C inhibitor) inhibitedlipopolysaccharide-stimulated but not basalcytokine-induced neutrophil chemoattractant production,while verapamil (a calcium channel blocker), TMB-8 (an inhibitor ofcalcium release from endoplasmic reticulum), and W7(calmodulin antagonist) completely abrogated thechemoattractant production. Altered intracellularcalcium, due to Ca2+ efflux from intracellularstores, may be involved in the “priming” ofmacrophages to release cytokine-induced neutrophilchemoattractant following triggering withlipopolysaccharide during acute cerulein pancreatitis. |
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GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE |
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Intracellular Calcium Affects Neutrophil Chemoattractant Expression by Macrophages in Rats with Cerulein-Induced Pancreatitis |
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http://dx.doi.org/10.1023/A:1018890703661 |
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Yamaguchi, Yasuo Akizuki, Eiji Matsumura, Fujio Okabe, Kazutoshi Liang, Jian Matsuda, Teishi Yamada, Shinwa Ogawa, Michio |
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