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. 2021 Feb 23;18(4):2187.
doi: 10.3390/ijerph18042187.

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

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

Janusz P Sikora et al. Int J Environ Res Public Health. .

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.

Keywords: ROS; SIRS; TNF-α receptor; neutrophils; respiratory burst.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Neutrophil respiratory burst after E.coli stimulation (in the studied children with sepsis (Group 1), burns (Group 2), and bone fractures (Group 3) at the time of diagnosis and in the control groups).
Figure 2
Figure 2
The rhodamine 123-fluorescence intensity of neutrophils without stimulation (control) [1] and exposed to Escherichia coli [2] and PMA [3] (in relative fluorescence units, i.e., the median channel of the fluorescing cell population).
Figure 3
Figure 3
Neutrophil respiratory burst after PMA stimulation (in the studied children with sepsis (Group 1), burns (Group 2), and bone fractures (Group 3) at the time of diagnosis and in the control groups).

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