Objectives: Children with meningococcal sepsis are highly at risk for fulminant disease, multiple organ failure, and death. Recently, neutrophil extracellular traps levels have been indicated as a marker for severity in different kinds of sepsis. Our aim was to study the role of neutrophil extracellular traposis in meninogococcal sepsis in children.
Design: We measured myeloperoxidase-DNA, a marker for neutrophil extracellular traps, in serum of meningococcal sepsis patients upon admission to PICU, at 24 hours, and at 1 month and studied the association with clinical outcome. Subsequently, we tested whether Neisseria meningitidis, isolated from children with meningococcal sepsis, were able to induce neutrophil extracellular traposis, using confocal microscopy live imaging.
Setting: We used enzyme-linked immunosorbent assays to measure myeloperoxidase-DNA in patient serum. We also included inflammatory markers that were previously measured in this group.
Patients: We included exclusively children with meningococcal sepsis.
Interventions: From each patient, serum was collected for analysis.
Measurements And Main Results: Myeloperoxidase-DNA levels at admission (n = 35; median, 0.21 AU/mL; interquartile range, 0.12-0.27) and at 24 hours (n = 39; median, 0.14 AU/mL; interquartile range, 0.09-0.25) were significantly higher than the myeloperoxidase-DNA levels after 1 month (controls: n = 36; median, 0.07 AU/mL; interquartile range, 0.05-0.09; p < 0.001). We did not observe a correlation between myeloperoxidase-DNA levels and mortality, cell-free DNA, or other inflammatory markers. In addition, N. meningitidis are fast and strong inducers of neutrophil extracellular traposis.
Conclusions: Children admitted to PICU for meningococcal sepsis have higher neutrophil extracellular traps levels at admission and after 24 hours than controls. Neutrophil extracellular traps levels were not associated with outcome, cell-free DNA, or other inflammatory markers. These neutrophil extracellular traps may be induced by N. meningitidis, since these are strong neutrophil extracellular traposis inducers.
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http://dx.doi.org/10.1097/PCC.0000000000001496 | DOI Listing |
Arch Immunol Ther Exp (Warsz)
January 2025
Department of Human Physiology, Medical University of Lublin, Lublin, Poland.
Systemic lupus erythematosus (SLE) is an autoimmune disease whose pathogenesis is not fully understood to date. One of the suggested mechanisms for its development is NETosis, which involves the release of a specific network consisting of chromatin, proteins, and enzymes from neutrophils, stimulating the immune system. One of its markers is citrullinated histone H3 (H3Cit).
View Article and Find Full Text PDFPLoS One
January 2025
Laboratório de Imunologia Celular (LIM-17), Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Background: NETosis is recognized as an important source of autoantigens. Therefore, we hypothesized whether the pristane-induced lupus mice model shows early activation of neutrophils, the presence of low-density granulocytes (LDGs), and neutrophil extracellular traps (NETs) release, which could contribute to the development of a lupus phenotype.
Methods: Twelve female wild-type Balb/c mice were intraperitoneally injected with pristane (n = 6; pristane group) or saline (n = 6; control group).
Shock
December 2024
Division of Trauma, Critical Care, and General Surgery, Department of Surgery, Mayo Clinic, 200 1st St. SW, Rochester, MN, United States 55905.
Background: Neutrophil extracellular traps (NETs), and its formation and release, known as NETosis, may play a role in the initiation of thrombin generation (TG) in trauma. The objective of this study was to assess whether trauma patients, who develop symptomatic venous thromboembolism (VTE), have increased levels of plasma citrullinated histone H3 (CitH3) and accelerated TG kinetics.
Methods: Patients presenting to a Level I Trauma Center as trauma activations had samples collected within 12 hours of time of injury (TOI), alongside healthy volunteers (HV).
Front Immunol
January 2025
Institute of Parasitology, Justus Liebig University Giessen, Giessen, Germany.
Bovine besnoitiosis is a re-emerging cattle disease caused by the apicomplexan parasite , which severely affects individual animal welfare and profitability in cattle industry. We recently showed that tachyzoite exposure to bovine polymorphonuclear neutrophils (PMN) effectively triggers neutrophil extracellular trap (NET) formation, leading to parasite immobilization hampering host cell infection. So far, the triggers of this defense mechanism remain unclear.
View Article and Find Full Text PDFMicrob Pathog
December 2024
MOE Joint International Research Laboratory of Animal Health and Food Safety, Nanjing Agricultural University, Nanjing 210095, PR China; College of Animal Science, Anhui Science and Technology University, Fengyang, 233100, PR China. Electronic address:
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