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dc.contributor.authorShields, Conor J
dc.contributor.authorO'Sullivan, Adrian W
dc.contributor.authorWang, Jiang H
dc.contributor.authorWinter, Desmond C
dc.contributor.authorKirwan, William O
dc.contributor.authorRedmond, H Paul
dc.date.accessioned2012-02-03T15:09:21Z
dc.date.available2012-02-03T15:09:21Z
dc.date.issued2012-02-03T15:09:21Z
dc.identifier.citationAnn Surg. 2003 Aug;238(2):249-57.en_GB
dc.identifier.issn0003-4932 (Print)en_GB
dc.identifier.issn0003-4932 (Linking)en_GB
dc.identifier.pmid12894019en_GB
dc.identifier.doi10.1097/01.sla.0000080827.77985.fcen_GB
dc.identifier.urihttp://hdl.handle.net/10147/208991
dc.description.abstractOBJECTIVE: This study sought to determine whether hypertonic saline (HTS) infusion modulates the host response to bacterial challenge. METHODS: Sepsis was induced in 30 Balb-C mice by intraperitoneal injection of Escherichia coli (5 x 107 organisms per animal). In 10 mice, resuscitation was performed at 0 and 24 hours with a 4 mL/kg bolus of HTS (7.5% NaCl), 10 animals received 4 mL/kg of normal saline (0.9% NaCl), and the remaining animals received 30 mL/kg of normal saline. Samples of blood, spleen, and lung were cultured at 8 and 36 hours. Polymorphonucleocytes were incubated in isotonic or hypertonic medium before culture with E. coli. Phagocytosis was assessed by flow cytometry, whereas intracellular bacterial killing was measured after inhibition of phagocytosis with cytochalasin B. Intracellular formation of free radicals was assessed by the molecular probe CM-H(2)DCFDA. Mitogen-activated protein (MAP) kinase p38 and ERK-1 phosphorylation, and nuclear factor kappa B (NFkappaB) activation were determined. Data are represented as means (SEM), and an analysis of variance test was performed to gauge statistical significance. RESULTS: Significantly reduced bacterial culture was observed in the animals resuscitated with HTS when compared with their NS counterparts, in blood (51.8 +/- 4.3 vs. 82.0 +/- 3.3 and 78.4 +/- 4.8, P = 0.005), lung (40.0 +/- 4.1 vs. 93.2 +/- 2.1 and 80.9 +/- 4.7, P = 0.002), and spleen (56.4 +/- 3.8 vs. 85.4 +/- 4.2 and 90.1 +/- 5.9, P = 0.05). Intracellular killing of bacteria increased markedly (P = 0.026) and superoxide generation was enhanced upon exposure to HTS (775.78 +/- 23.6 vs. 696.57 +/- 42.2, P = 0.017) despite inhibition of MAP kinase and NFkappaB activation. CONCLUSIONS: HTS significantly enhances intracellular killing of bacteria while attenuating receptor-mediated activation of proinflammatory cascades.
dc.language.isoengen_GB
dc.subject.meshAnalysis of Varianceen_GB
dc.subject.meshAnimalsen_GB
dc.subject.meshComputer Graphicsen_GB
dc.subject.meshDisease Models, Animalen_GB
dc.subject.meshEnzyme Activationen_GB
dc.subject.meshEscherichia coli Infections/*therapyen_GB
dc.subject.meshHumansen_GB
dc.subject.meshMaleen_GB
dc.subject.meshMiceen_GB
dc.subject.meshMice, Inbred BALB Cen_GB
dc.subject.meshMitogen-Activated Protein Kinase Kinases/metabolismen_GB
dc.subject.meshNF-kappa B/metabolismen_GB
dc.subject.meshNeutrophils/*metabolismen_GB
dc.subject.meshPhagocytosis/drug effectsen_GB
dc.subject.meshRandom Allocationen_GB
dc.subject.meshSaline Solution, Hypertonic/*therapeutic useen_GB
dc.subject.meshSuperoxides/*metabolismen_GB
dc.subject.meshSurvival Analysisen_GB
dc.titleHypertonic saline enhances host response to bacterial challenge by augmenting receptor-independent neutrophil intracellular superoxide formation.en_GB
dc.contributor.departmentDepartment of Academic Surgery, Cork University Hospital and National University , of Ireland, Cork, Ireland.en_GB
dc.identifier.journalAnnals of surgeryen_GB
dc.description.provinceMunster
html.description.abstractOBJECTIVE: This study sought to determine whether hypertonic saline (HTS) infusion modulates the host response to bacterial challenge. METHODS: Sepsis was induced in 30 Balb-C mice by intraperitoneal injection of Escherichia coli (5 x 107 organisms per animal). In 10 mice, resuscitation was performed at 0 and 24 hours with a 4 mL/kg bolus of HTS (7.5% NaCl), 10 animals received 4 mL/kg of normal saline (0.9% NaCl), and the remaining animals received 30 mL/kg of normal saline. Samples of blood, spleen, and lung were cultured at 8 and 36 hours. Polymorphonucleocytes were incubated in isotonic or hypertonic medium before culture with E. coli. Phagocytosis was assessed by flow cytometry, whereas intracellular bacterial killing was measured after inhibition of phagocytosis with cytochalasin B. Intracellular formation of free radicals was assessed by the molecular probe CM-H(2)DCFDA. Mitogen-activated protein (MAP) kinase p38 and ERK-1 phosphorylation, and nuclear factor kappa B (NFkappaB) activation were determined. Data are represented as means (SEM), and an analysis of variance test was performed to gauge statistical significance. RESULTS: Significantly reduced bacterial culture was observed in the animals resuscitated with HTS when compared with their NS counterparts, in blood (51.8 +/- 4.3 vs. 82.0 +/- 3.3 and 78.4 +/- 4.8, P = 0.005), lung (40.0 +/- 4.1 vs. 93.2 +/- 2.1 and 80.9 +/- 4.7, P = 0.002), and spleen (56.4 +/- 3.8 vs. 85.4 +/- 4.2 and 90.1 +/- 5.9, P = 0.05). Intracellular killing of bacteria increased markedly (P = 0.026) and superoxide generation was enhanced upon exposure to HTS (775.78 +/- 23.6 vs. 696.57 +/- 42.2, P = 0.017) despite inhibition of MAP kinase and NFkappaB activation. CONCLUSIONS: HTS significantly enhances intracellular killing of bacteria while attenuating receptor-mediated activation of proinflammatory cascades.


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