Hypertonic Saline Solution Drives Neutrophil from Bystander Organ to Infectious Site in Polymicrobial Sepsis: A Cecal Ligation and Puncture Model

Theobaldo, Mariana Cardillo; Llimona, Flávia; Petroni, Ricardo; Rios, Ester Correia Sarmento; Velasco, Irineu Tadeu; Soriano, Francisco Garcia

doi:10.1371/journal.pone.0074369

Cited by 15 publications

(11 citation statements)

References 37 publications

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“…Tumor necrosis factor-! and IL-1" are considered pivotal mediators of lung inflammation in acute respiratory distress syndrome (ARDS) (13,24). The release of TNF-!…”

Section: Discussionmentioning

confidence: 99%

“…Thus, in the present study, we investigated whether the failure of neutrophil migration in sepsis and distant organ infiltration were prevented by LPS tolerance. The cecal ligation and puncture (CLP) model was selected for this study because it closely resembles the course of human sepsis (23,24). Here we report that LPS tolerance is associated with a substantial reduction in distant organ damage (lung) and sustained ability for neutrophil infiltration at the infectious site (peritoneal) after CLP challenge.…”

Section: Introductionmentioning

confidence: 99%

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Endotoxin Tolerance Drives Neutrophil To Infectious Site

Ariga

Abatepaulo

Melo

et al. 2014

Shock

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The objective of this randomized animal study and laboratory investigation was to investigate whether lipopolysaccharide tolerance redirects neutrophil migration between organs. Male BALB/c mice received subcutaneous injections of lipopolysaccharide (1 mg/kg) for 5 days, followed by cecal ligation and puncture (CLP). Cytokines and adhesion molecules were measured after tolerance and CLP challenge. Increased numbers of neutrophils were observed in the peritoneal cavity of tolerant mice, which was associated with increased levels of adhesion molecules and chemokines. In contrast, nontolerant mice accumulated higher numbers of neutrophils in the lungs compared with those in the peritoneal cavity. Neutrophil function accessed by hydrogen peroxide production from neutrophils recovered from peritoneal cavity showed that tolerance increased the capacity to produce hydrogen peroxide. Mortality was reduced in tolerant animals. This study demonstrated that tolerance reduces leukocyte accumulation in the lung after CLP by redirecting neutrophils to the site of infection.

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“…Tumor necrosis factor-! and IL-1" are considered pivotal mediators of lung inflammation in acute respiratory distress syndrome (ARDS) (13,24). The release of TNF-!…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Endotoxin Tolerance Drives Neutrophil To Infectious Site

Ariga

Abatepaulo

Melo

et al. 2014

Shock

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“…20 In spite of an inhibitory effect on neutrophil function, Bahrami et al 27 report that in a murine model of very severe hemorrhagic shock, with arterial blood pressure reduced to and kept at 30-35 mm Hg for two hours, no reduction in mortality was observed following hypertonic saline, or hypertonic saline plus hydroxyl ethyl starch. Theobaldo et al, 28 employed a mouse model of cecal ligation and puncture and showed that hypertonic saline drives neutrophils from bystander organs to an infectious site in polymicrobial sepsis: a cecal ligation and puncture model.…”

Section: Neutrophil Functionmentioning

confidence: 99%

Hypertonic saline for treatment of shock: have we looked for everything?

Silva

2014

Medical Express

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This review is dedicated to the memory of Luis Poli de Figueiredo, who is responsible for much of what we know about small volume resuscitation. Small volume hypertonic resuscitation was originally based on the concept that a physiologically significant blood volume expansion follows the administration of a comparatively small volume of hypertonic fluid. Because hypertonicity is a physiological vasodilator, its use after severe blood loss induces reperfusion. Previously reported research disclosed a number of additional properties of hypertonic NaCl, amongst them (i) the correction of endothelial and red cell edema with significant consequences in terms of capillary blood flow; (ii) modulation of the immune system, with applications repercussions in the field of sepsis. This review covers developments in this field that occurred from 2005 through 2013. We discuss the discrepancy between animal experiments and human trials, and argue that the basic objective of most multicenter clinical trials may have been based upon a poor strategy.K EYWORDS: Shock; Hemorrhage; Sepsis Hypertonic saline; Immune circulation.Rocha-e-Silva M. Hypertonic saline for treatment of shock: have we looked for everything? MEDICALEXPRESS. 2014;1(1):14-21.

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“…Experimental studies are confident about the benefits of hypertonic solution use (6)(7)(8). Previous studies have shown that a hypertonic solution reduces the inflammatory profile of endotoxemia in septic mice, as well as pulmonary fibrosis (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies have shown that a hypertonic solution reduces the inflammatory profile of endotoxemia in septic mice, as well as pulmonary fibrosis (7)(8)(9). Although the use of hypertonic saline resuscitation presents benefits in controlling the inflammatory process and in reducing mortality in experimental models, clinical trials have failed to demonstrate these same effects (10,11).…”

Section: Introductionmentioning

confidence: 99%

Impact of Time on Fluid Resuscitation with Hypertonic Saline (NaCl 7.5%) in Rats with LPS-Induced Acute Lung Injury

Petroni

Biselli²,

Lima³

et al. 2015

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Acute lung injury (ALI) is a common complication associated with septic shock that directly influences the prognosis of sepsis patients. Currently, one of the main supportive treatment modalities for septic shock is fluid resuscitation. The use of hypertonic saline (HS: 7.5% NaCl) for fluid resuscitation has been described as a promising therapy in experimental models of sepsis-induced ALI, but it has failed to produce similar results in clinical practice. Thus, we compared experimental timing versus clinical timing effectiveness (i.e., early vs. late fluid resuscitation) after the inflammatory scenario was established in a rat model of bacterial lipopolysaccharide-induced ALI. We found that late fluid resuscitation with hypertonic saline (NaCl 7.5%) did not reduce the mortality rates of animals compared with the mortality late associated with early treatment. Late fluid resuscitation with both hypertonic and normal saline increased pulmonary inflammation, decreased pulmonary function, and induced pulmonary injury by elevating metalloproteinase-2 and metalloproteinase-9 activity and collagen deposition in the animals, unlike early treatment. The animals with lipopolysaccharide-induced ALI that received late resuscitation with any kind of fluids demonstrated aggravated pulmonary injury and respiratory function. Moreover, we showed that the therapeutic window for a beneficial effect of fluid resuscitation with hypertonic saline is very narrow.

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Hypertonic Saline Solution Drives Neutrophil from Bystander Organ to Infectious Site in Polymicrobial Sepsis: A Cecal Ligation and Puncture Model

Cited by 15 publications

References 37 publications

Endotoxin Tolerance Drives Neutrophil To Infectious Site

Endotoxin Tolerance Drives Neutrophil To Infectious Site

Hypertonic saline for treatment of shock: have we looked for everything?

Impact of Time on Fluid Resuscitation with Hypertonic Saline (NaCl 7.5%) in Rats with LPS-Induced Acute Lung Injury

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