Respiratory Burst and TNF-α Receptor Expression of Neutrophils after Sepsis and Severe Injury-Induced Inflammation in Children.

Janusz P Sikora,Dariusz Zawadzki,Monika Burzyńska,Jarosław Sobczak,Przemysław Przewratil,Anna Wysocka

doi:10.3390/ijerph18042187

Abstract

Systemic inflammatory response syndrome (SIRS) is defined as the systemic host response to infection or a non-infectious factor. The purpose of this study was to evaluate the involvement of reactive oxygen species (ROS) in severe inflammation and to assess the discrimination strength of the neutrophil BURSTTEST assay regarding its etiology in three groups of patients (sepsis, burns, and bone fractures) who met the SIRS criteria. The neutrophil activation (respiratory burst of granulocytes as well as p55 and p75 tumor necrosis factor (TNF-α) receptor expression) was evaluated twice using flow cytometry, and the results were compared with healthy controls and among SIRS subjects. A decreased oxygen metabolism in neutrophils after E. coli stimulation and increased TNF-α receptor expression were found in septic and burned patients on admission, while ROS production augmented and TNF-α receptor expression diminished with the applied therapy. The significant differences in neutrophil respiratory burst intensity among septic and burned patients and those with sepsis and bone fractures were found (however, there were not any such differences between patients with thermal and mechanical injuries). This study indicates that the neutrophil BURSTTEST evaluation might be a clinically reliable marker for differentiating the SIRS etiology.

Highlights

Introduction published maps and institutional affilSepsis and severe injuries are known to be common causes of morbidity and mortality in critically ill children
Our study indicates that the neutrophil BURSTTEST evaluation might be considered as a reliable marker for differentiating the Systemic inflammatory response syndrome (SIRS) etiology
Significant differences were revealed in the neutrophil respiratory burst intensity after E. coli stimulation assessed in 3 groups of patients, both prior to treatment (p = 0.0029) as well as after its completion and C-reactive protein (CRP) normalization (p = 0.0001)

Summary

Introduction

Introduction published maps and institutional affilSepsis and severe injuries are known to be common causes of morbidity and mortality in critically ill children. In the case of an unfavorable and uncontrolled protective systemic reaction of the host, the excessively released endogenic inflammation mediators (e.g., cytokines and ROS) cause various tissue damage and result in the development of multiple organ dysfunction syndrome (MODS). This syndrome is thought to be the most severe complication of systemic inflammatory response syndrome (SIRS), independently of the acted stimulus. A so-called “respiratory burst” of neutrophils, which is a consequence of the activation of leukocytes, dendritic cells, and vascular endothelium, is considered the basis of SIRS pathogenesis during sepsis or severe injuries [1,2,3,4,5]. Stimulation of these cells and their interaction is possible due to iations

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