Inflammation Assays

  • Respiratory Burst (ROS, Phagoburst)
  • NETs
  • Phagocytosis/trogocytosis

Therapeutic blocking of NETosis and enhancement of neutrophil phagocytosis/trogocytosis

Neutrophils are armed with a variety of effector mechanisms, they release neutrophil extracellular traps (NETs), comprising of chromatin and antimicrobial proteins which are released via a unique, pro-inflammatory form of cell death called NETosis. Dysregulated NET release can damage the host, contributing to autoimmune diseases such as Systemic Lupus Erythematosus (SLE) by the release of autoantigens. Similarly, dysregulated NET release contributes to diseases such as atherosclerosis, deep vein thrombosis and has been shown to promote cancer progression and metastasis. Modulating neutrophil function is therefore a potential therapeutic intervention.

Figure A. Neutrophils were isolated from fresh blood, incubated with the NOX2 inhibitor (DPI) and then stimulated with PMA in the presence of SYTOX green to detect NETs. Cells were imaged for green fluorescence (NETs) every 30 minutes for 4 hours. Data shows that NETosis increases over time and is inhibited by DPI.
Figure B: Phagocytosis - Neutrophils were cultured with pHrodo labelled E. coli in the presence or absence of a titration of cytochalasin D and phagocytosis measured by flow cytometry. Phagocytic neutrophils were identified as CD66b+ pHrodo+.

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