Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies · 2012
Prophylactic zinc supplementation reduces bacterial load and improves survival in a murine model of sepsis.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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Nowak Jeffrey E, Harmon Kelli, Caldwell Charles C, Wong Hector R
Аннотация
OBJECTIVE: We previously demonstrated that altered zinc homeostasis is an important feature of pediatric sepsis, thus raising the possibility of zinc supplementation as a therapeutic strategy in sepsis. Herein, we tested the hypothesis that prophylactic zinc supplementation would be beneficial in a murine model of peritoneal sepsis.
DESIGN: Murine model of sepsis (intraperitoneal fecal-slurry injection).
SETTING: Basic science research laboratory.
SUBJECTS: C57BL/6 male mice.
INTERVENTIONS: Intraperitoneal fecal-slurry injection, with or without zinc supplementation (10 mg/kg of intraperitoneal zinc gluconate for 3 days prior to intraperitoneal fecal-slurry injection).
MEASUREMENTS AND MAIN RESULTS: Survival over 3 days following intraperitoneal fecal-slurry injection, markers of inflammation, bacterial load studies, and immunophenotyping studies. Zinc-supplemented mice demonstrated a significant survival advantage compared to control (nonsupplemented) mice. Zinc-supplemented mice also demonstrated moderate reductions of inflammation and immune activation. The survival advantage primarily correlated with reduced in vivo bacterial load in zinc-supplemented mice, compared to controls. In addition, peritoneal macrophages harvested from zinc-supplemented mice demonstrated a significantly enhanced phagocytosis capacity for Escherichia coli and Staphylococcus aureus, compared to peritoneal macrophages harvested from control mice.
CONCLUSION: Prophylactic zinc supplementation reduces bacterial load and is beneficial in a murine model of peritoneal sepsis.
DESIGN: Murine model of sepsis (intraperitoneal fecal-slurry injection).
SETTING: Basic science research laboratory.
SUBJECTS: C57BL/6 male mice.
INTERVENTIONS: Intraperitoneal fecal-slurry injection, with or without zinc supplementation (10 mg/kg of intraperitoneal zinc gluconate for 3 days prior to intraperitoneal fecal-slurry injection).
MEASUREMENTS AND MAIN RESULTS: Survival over 3 days following intraperitoneal fecal-slurry injection, markers of inflammation, bacterial load studies, and immunophenotyping studies. Zinc-supplemented mice demonstrated a significant survival advantage compared to control (nonsupplemented) mice. Zinc-supplemented mice also demonstrated moderate reductions of inflammation and immune activation. The survival advantage primarily correlated with reduced in vivo bacterial load in zinc-supplemented mice, compared to controls. In addition, peritoneal macrophages harvested from zinc-supplemented mice demonstrated a significantly enhanced phagocytosis capacity for Escherichia coli and Staphylococcus aureus, compared to peritoneal macrophages harvested from control mice.
CONCLUSION: Prophylactic zinc supplementation reduces bacterial load and is beneficial in a murine model of peritoneal sepsis.