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

2021 ◽  
Vol 18 (4) ◽  
pp. 2187
Author(s):  
Janusz P. Sikora ◽  
Jarosław Sobczak ◽  
Dariusz Zawadzki ◽  
Przemysław Przewratil ◽  
Anna Wysocka ◽  
...  
Keyword(s):  
Respiratory Burst ◽  
Host Response ◽  
Bone Fractures ◽  
Oxygen Metabolism ◽  
Receptor Expression ◽  
Burst Intensity ◽  
Tnf Α ◽  
Reliable Marker ◽  
Neutrophil Respiratory Burst ◽  
Necrosis Factor

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.

fMLP-stimulated release of reactive oxygen species from adherent leukocytes increases microvessel permeability

2006 ◽  
Vol 290 (1) ◽  
pp. H365-H372 ◽  
Author(s):  
Longkun Zhu ◽  
Pingnian He
Keyword(s):  
Reactive Oxygen Species ◽  
Respiratory Burst ◽  
Leukocyte Adhesion ◽  
Autologous Blood ◽  
Blood Perfusion ◽  
Oxygen Species ◽  
Tnf Α ◽  
Microvessel Permeability ◽  
Adherent Leukocytes ◽  
Neutrophil Respiratory Burst

Our previous study ( Am J Physiol Heart Circ Physiol 288: H1331–H1338, 2005) demonstrated that TNF-α induced significant leukocyte adhesion without causing increases in microvessel permeability, and that formyl-Met-Leu-Phe-OH (fMLP)-stimulated neutrophils in the absence of adhesion increased microvessel permeability via released reactive oxygen species (ROS). The objective of our present study is to investigate the mechanisms that regulate neutrophil respiratory burst and the roles of fMLP-stimulated ROS release from adherent leukocytes in microvessel permeability. A technique that combines single-microvessel perfusion with autologous blood perfusion was employed in venular microvessels of rat mesenteries. Leukocyte adhesion was induced by systemic application of TNF-α. Microvessel permeability was assessed by measuring hydraulic conductivity ( Lp). The 2-h autologous blood perfusion after TNF-α application increased leukocyte adhesion from 1.2 ± 0.2 to 13.3 ± 1.6 per 100 μm of vessel length without causing increases in Lp. When fMLP (10 μM) was applied to either perfusate ( n = 5) or superfusate ( n = 8) in the presence of adherent leukocytes, Lptransiently increased to 4.9 ± 0.9 and 4.4 ± 0.3 times the control value, respectively. Application of superoxide dismutase or an iron chelator, deferoxamine mesylate, after fMLP application prevented or attenuated the Lpincrease. Chemiluminescence measurements in isolated neutrophils demonstrated that TNF-α alone did not induce ROS release but that preexposure of neutrophils to TNF-α in vivo or in vitro potentiated fMLP-stimulated ROS release. These results suggest a priming role of TNF-α in fMLP-stimulated neutrophil respiratory burst and indicate that the released ROS play a key role in leukocyte-mediated permeability increases during acute inflammation.

Neonatal rat microglia derived from different brain regions have distinct activation responses

2011 ◽  
Vol 7 (1) ◽  
pp. 5-16 ◽  
Author(s):  
Aaron Y. Lai ◽  
Kamaldeep S. Dhami ◽  
Comfort D. Dibal ◽  
Kathryn G. Todd
Keyword(s):  
Purinergic Receptor ◽  
Brain Regions ◽  
Receptor Expression ◽  
Neonatal Rat ◽  
Regional Heterogeneity ◽  
Tnf Α ◽  
Old Rats ◽  
Factor Α ◽  
Induced Changes ◽  
Necrosis Factor

The regional heterogeneity of neuronal phenotypes is a well-known phenomenon. Whether or not glia derived from different brain regions are phenotypically and functionally distinct is less clear. Here, we show that microglia, the resident immune cells of the brain, display region-specific responses for activating agents including glutamate (GLU), lipopolysaccharide (LPS) and adenosine 5′-triphosphate (ATP). Primary microglial cultures were prepared from brainstem (Brs), cortex (Ctx), hippocampus (Hip), striatum (Str) and thalamus (Thl) of 1-day-old rats and were shown to upregulate the release of nitric oxide (NO) and brain-derived neurotrophic factor (BDNF) in a region- and activator-specific manner. With respect to ATP specifically, ATP-induced changes in microglial tumor necrosis factor-α (TNF-α) release, GLU uptake and purinergic receptor expression were also regionally different. When co-cultured with hypoxia (Hyp)-injured neurons, ATP-stimulated microglia from different regions induced different levels of neurotoxicity. These region-specific responses could be altered by pre-conditioning the microglia in a different neurochemical milieu, with taurine (TAU) being one of the key molecules involved. Together, our results demonstrate that microglia display a regional heterogeneity when activated, and this heterogeneity likely arises from differences in the environment surrounding the microglia. These findings present an additional mechanism that may help to explain the regional selectiveness of various brain pathologies.

Exposure to febrile temperature upregulates expression of pyrogenic cytokines in endotoxin-challenged mice

1999 ◽  
Vol 276 (6) ◽  
pp. R1653-R1660 ◽  
Author(s):  
Qingqi Jiang ◽  
Louis Detolla ◽  
Ishwar S. Singh ◽  
Lisa Gatdula ◽  
Bridget Fitzgerald ◽  
...  
Keyword(s):  
Core Temperature ◽  
Host Response ◽  
Peak Plasma ◽  
Thermal Component ◽  
Multiple Organs ◽  
Acute Infections ◽  
Tnf Α ◽  
Factor Α ◽  
Kinetics Of ◽  
Necrosis Factor

Fever is a phylogenetically ancient response that is associated with improved survival in acute infections. In endothermic animals, fever is induced by a set of pyrogenic cytokines [tumor necrosis factor-α (TNF-α), interleukin (IL)-1, and IL-6] that are also essential for survival in acute infections. We studied the influence of core temperature on cytokine expression using an anesthetized mouse model in which core temperature was adjusted by immersion in water baths. We showed that raising core temperature from basal (36.5–37.5°C) to febrile (39.5–40°C) levels increased peak plasma TNF-α and IL-6 levels by 4.1- and 2.7-fold, respectively, and changed the kinetics of IL-1β expression in response to lipopolysaccharide challenge. TNF-α levels were increased predominantly in liver, IL-1β levels were higher in lung, and IL-6 levels were widely increased in multiple organs in the warmer mice. This demonstrates that the thermal component of fever may directly contribute to shaping the host response by regulating the timing, magnitude, and tissue distribution of cytokine generation during the acute-phase response.

Endotoxin, tumor necrosis factor, and dexamethasone effects on human endothelial cell fibronectin dynamics: synthesis, matrix assembly, and receptor expression

1995 ◽  
Vol 73 (7-8) ◽  
pp. 515-524 ◽  
Author(s):  
Lewis H. Romer ◽  
Richard A. Polin
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cell ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Receptor Expression ◽  
Matrix Assembly ◽  
Down Regulation ◽  
Cell Extracts ◽  
Tnf Α ◽  
Necrosis Factor

The three inflammatory modulators endotoxin, tumor necrosis factor (TNF) α, and dexamethasone (DEX) were studied for their effects on fibronectin (FN) dynamics in human umbilical vein endothelial cells. Cell culture supernatants were analyzed for new soluble pool FN synthesis. Endotoxin (LPS) (10 μg/mL) decreased the newly synthesized soluble pool of FN (p < 0.05). An increase in soluble FN was demonstrated with 1 and 10 ng/mL TNF α (p < 0.05). DEX decreased newly synthesized endothelial cell (EC) FN in the soluble pool at 4, 40, and 400 μg/mL (p < 0.05). Extracellular matrix FN content was examined using immunofluorescence. The thick FN mesh seen in control cells contrasted with a decreased FN matrix after treatment with each of the three study agents. Immunoprecipitation of the FN receptor α5β1 integrin from [35S]methionine-labelled cell extracts demonstrated down regulation of receptor expression by both TNF α and DEX as compared with control samples. These data indicate that LPS, TNF α, and DEX may weaken EC–substratum adhesion by differential effects on FN synthesis and secretion, FN incorporation into the extracellular matrix, and down regulation of FN receptor expression.Key words: endothelium, fibronectin, extracellular matrix, integrin, cytokine.

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