Effect of polyclonal immunoglobulins on neutrophil phagocytic capacity and reactive oxygen production in patients with gram-negative septicemia

Wenisch, Christoph; Parschalk, Bernhard; Patruta, Sandra; Brustbauer, R.; Graninger, Wolfgang

doi:10.1007/bf02561525

Cited by 21 publications

(13 citation statements)

References 25 publications

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“…Our findings are in agreement with previous reports showing a high ROS generation in critically ill patients that developed sepsis (17). However, Wenisch et al (18) found a decreased ROS generation in patients with gram-negative sepsis, corroborating their previous results. Respiratory burst is one of the most important neutrophil defenses to control bacterial infection (6).…”

Section: Discussionsupporting

confidence: 95%

“…This result is supported by previously reported findings in patients with sepsis (21) and is in agreement with data showing that primed neutrophils from healthy volunteers present an enhanced phagocytosis activity (10). On the other hand, studies using E. coli as stimulus showed a decreased phagocytosis in patients with gramnegative sepsis (18).…”

Section: Discussionsupporting

confidence: 93%

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Upregulation of Reactive Oxygen Species Generation and Phagocytosis, and Increased Apoptosis in Human Neutrophils During Severe Sepsis and Septic Shock

Martins¹,

Kallas²,

Neto

et al. 2003

Shock

141

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We evaluated neutrophil activation by measuring its phagocytic ability and oxidative burst activity in 16 patients with sepsis and 16 healthy volunteers. We also focused on neutrophil apoptosis as a regulatory mechanism of the inflammatory response. Neutrophil phagocytosis was evaluated by the detection of propidium iodide (PI)-labeled Staphylococcus aureus added to whole blood. Reactive oxygen species (ROS) formation was quantified by measuring the oxidation of 2',7' dichlorofluorescein diacetate (DCFH-DA) at baseline and after cell stimulation with phorbol myristate acetate (PMA), and bacterial cells (killed S. aureus) or products (lipopolysaccharide [LPS] and N-formyl-methionyl-leucyl-phenylalanine [FMLP]). Apoptosis was assessed in neutrophils stained with annexin V and PI. Neutrophil phagocytic ability was increased in patients with sepsis compared with healthy controls (median geometric mean fluorescence intensity [GMFI] was 101.9 and 54.7, respectively; P = 0.05). ROS formation was enhanced in patients with sepsis compared with healthy volunteers at baseline (median GMFI 275.6 and 52.1, respectively; P < 0.001), and after stimulation with S. aureus (median GMFI 2395.8 and 454.9, respectively; P < 0.001), PMA (median GMFI 1120.6 and 307.5, respectively; P = 0.003), FMLP (median GMFI 792.4 and 123.2, respectively; P < 0.001), and LPS (median GMFI 624.8 and 144.8, respectively; P < 0.001). Early neutrophil apoptosis was increased in patients with sepsis compared with healthy volunteers (median 11.3% and 9.1%, respectively; P = 0.03). These data demonstrate that neutrophil function is enhanced in patients with sepsis. Additionally, circulating neutrophils from patients with sepsis presented with increased early apoptosis, which may be consequence of a regulatory mechanism of the inflammatory response.

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Section: Discussionsupporting

confidence: 95%

Section: Discussionsupporting

confidence: 93%

Upregulation of Reactive Oxygen Species Generation and Phagocytosis, and Increased Apoptosis in Human Neutrophils During Severe Sepsis and Septic Shock

Martins¹,

Kallas²,

Neto

et al. 2003

Shock

141

View full text Add to dashboard Cite

show abstract

“…Moreover, Lima et al (53) have reported that autophagy and phagocytosis are interdependent and complementary to each other. A decrease in phagocytosis by neutrophils was observed as a result of E. coli -induced sepsis in humans by Wenisch et al (54). In another study, Krasnodembskaya et al (55) have reported an increase in phagocytosis as a result of intervention with mesenchymal stem cells in mice with sepsis.…”

Section: Discussionmentioning

confidence: 94%

Deletion of Nlrp3 Augments Survival during Polymicrobial Sepsis by Decreasing Autophagy and Enhancing Phagocytosis

Jin

Batra

Jeyaseelan

2017

The Journal of Immunology

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NLRP3 inflammasome is a critical player in innate immunity. Neutrophil recruitment to tissues and effective function of neutrophils are critical innate immune function to bacterial clearance. However, the role of NLRP3 in neutrophil-dependent bacterial clearance in polymicrobial sepsis is unclear. Herein, we evaluated the role of NLRP3 in polymicrobial sepsis induced by cecal ligation and puncture (CLP). Our results exhibit protection from death in NLRP3-deficient (Nlrp3−/−) and NLRP3 inhibitor-treated wild-type (C57Bl/6) mice. Both Nlrp3−/− and NLRP3 inhibitor-treated mice displayed lower bacterial load albeit no impairment in neutrophil recruitment to peritoneum. However, neutrophil depletion abrogated protection from death of nd NLRP3-deficient (Nlrp3−/−) mice in response to CLP. Intriguingly, Nlrp3−/− peritoneal cells (primarily neutrophils) following CLP demonstrate decreased autophagy, augmented phagocytosis and enhanced scavenger receptor (MARCO) and mannose binding leptin (MBL) expression. These findings enhance our understanding of the critical role of NLRP3 in modulating autophagy and phagocytosis in neutrophils and suggest that therapies should be targeted to modulate both autophagy and phagocytosis in neutrophils to control bacterial burden in tissues during CLP-induced polymicrobial sepsis.

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“…In this study, we investigated whether an increased resting burst in patients with liver cirrhosis is associated with an impaired respiratory burst capacity in response to bacteria. We hypothesized that, in the presence of subclinical endotoxaemia and clinically manifested infection, phagocytes are less responsive to Escherichia coli and their respiratory burst capacity becomes exhausted, as has been demonstrated previously for critically ill non-cirrhotic patients with systemic inflammatory response syndrome (SIRS) [29] and Gramnegative septicaemia [30]. To confirm our hypothesis and to determine the significance of elevated ROS production, the endotoxaemia marker LBP [31], the acute-phase reactant C-reactive protein (CRP) and immunoglobulin (Ig)G autoantibodies against oxidized low-density lipoproteins as a marker of lipid peroxidation in vivo [32,33] were correlated with respiratory burst activity in neutrophils and monocytes from patients with liver cirrhosis.…”

Section: Introductionmentioning

confidence: 98%

The augmented neutrophil respiratory burst in response toEscherichia coliis reduced in liver cirrhosis during infection

Bruns

Peter

Hagel

et al. 2011

Clinical and Experimental Immunology

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SummarySeveral functional abnormalities in phagocytes from patients with liver cirrhosis contribute to an increased risk of infection. An increased resting respiratory burst has been observed in neutrophils from cirrhotic patients. We investigated whether an infection in cirrhosis affects the respiratory burst capacity of neutrophils and monocytes in response to Escherichia coli. This study included 45 hospitalized patients with liver cirrhosis and clinical signs of infection, 39 patients with liver cirrhosis in the absence of infection and 29 healthy subjects. Respiratory burst, lipopolysaccharide-binding protein (LBP), and immunoglobulin (Ig)G-autoantibodies against oxidized lowdensity lipoproteins (ab-oxLDL) were measured. The fraction of neutrophils spontaneously producing reactive oxygen species (ROS) was elevated in liver cirrhosis (P < 0·01). The neutrophil resting burst increased with Child-Pugh stage (P = 0·02) and correlated with augmented ROS release in response to opsonized E. coli (P < 0·05). Although LBP was increased in patients with cirrhosis (P < 0·01), higher LBP levels correlated with a lower resting burst in neutrophils (rs = -0·395; P < 0·01). In the presence of infection, the resting burst was unaltered. However, neutrophil ROS release in response to E. coli was reduced markedly (P = 0·01), and it decreased as serum C-reactive protein (CRP) concentration rose (rs = -0·437; P < 0·01), indicating the development of a sepsis-like immune paralysis. A positive correlation between ab-oxLDL and ROS release was observed (P < 0·01). In conclusion, the respiratory burst increases with severity of liver cirrhosis but is restrained by increasing LBP levels. Augmented ROS release in response to E. coli is accompanied by elevated markers of oxidative damage and becomes exhausted in the presence of infection.

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Effect of polyclonal immunoglobulins on neutrophil phagocytic capacity and reactive oxygen production in patients with gram-negative septicemia

Cited by 21 publications

References 25 publications

Upregulation of Reactive Oxygen Species Generation and Phagocytosis, and Increased Apoptosis in Human Neutrophils During Severe Sepsis and Septic Shock

Upregulation of Reactive Oxygen Species Generation and Phagocytosis, and Increased Apoptosis in Human Neutrophils During Severe Sepsis and Septic Shock

Deletion of Nlrp3 Augments Survival during Polymicrobial Sepsis by Decreasing Autophagy and Enhancing Phagocytosis

The augmented neutrophil respiratory burst in response toEscherichia coliis reduced in liver cirrhosis during infection

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