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    Hypertonic saline enhances host response to bacterial challenge by augmenting receptor-independent neutrophil intracellular superoxide formation.

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    Authors
    Shields, Conor J
    O'Sullivan, Adrian W
    Wang, Jiang H
    Winter, Desmond C
    Kirwan, William O
    Redmond, H Paul
    Affiliation
    Department of Academic Surgery, Cork University Hospital and National University , of Ireland, Cork, Ireland.
    Issue Date
    2012-02-03T15:09:21Z
    MeSH
    Analysis of Variance
    Animals
    Computer Graphics
    Disease Models, Animal
    Enzyme Activation
    Escherichia coli Infections/*therapy
    Humans
    Male
    Mice
    Mice, Inbred BALB C
    Mitogen-Activated Protein Kinase Kinases/metabolism
    NF-kappa B/metabolism
    Neutrophils/*metabolism
    Phagocytosis/drug effects
    Random Allocation
    Saline Solution, Hypertonic/*therapeutic use
    Superoxides/*metabolism
    Survival Analysis
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    Citation
    Ann Surg. 2003 Aug;238(2):249-57.
    Journal
    Annals of surgery
    URI
    http://hdl.handle.net/10147/208991
    DOI
    10.1097/01.sla.0000080827.77985.fc
    PubMed ID
    12894019
    Abstract
    OBJECTIVE: 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.
    Language
    eng
    ISSN
    0003-4932 (Print)
    0003-4932 (Linking)
    ae974a485f413a2113503eed53cd6c53
    10.1097/01.sla.0000080827.77985.fc
    Scopus Count
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    Cork University Hospital

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