Neutrophil activation and neutrophil derived neutrophil extracellular trap formation in patients with coronary artery ectasia

Abstract

Background: This study investigated neutrophil activation and neutrophil-derived extracellular traps formation in coronary artery ectasia. Methods: We enrolled 90 patients who underwent coronary angiography, and included 30 patients with coronary artery ectasia (CAE), 30 patients with obstructive coronary artery disease (CAD) and 30 patients with normal coronary arteries (CON). Intra-neutrophil mean myeloperoxidase index (MPXI) was determined using an automated blood cell counter (ADVIA2120 Hematology System). Serum concentrations of plasma adhesion molecules, cytokines, and neutrophil-derived extracellular traps were quantified. Results: The intra-neutrophil mean myeloperoxidase index was reduced in CAE patients compared to CAD and CON patients (1.02 ± 3.01, 3.22 ± 3.03, 3.52 ± 4.25, respectively; CAE vs CAD, p = 0.016 and CAE vs CON, p = 0.007). Multiple logistic regression analysis showed that MPXI and dsDNA were independent factors that predicted the presence of CAE. CAE patients had higher levels of plasma adhesion molecules (P-selectin glycoprotein ligand-1, Eselectin, L-selectin) and interleukin 1 beta levels. Neutrophil extracellular trap concentrations were significantly higher in the CAE group compared to CAD and CON patients (284.31(258.33-449.91) ng/mL, 225.12(203.34-257.13) ng/mL, and 247.37(231.04-273.01) ng/mL, respectively; CAE vs CAD, p = 0.000 and CAE vs CON, p = 0.001). Conclusions: Peripheral neutrophils from CAE patients were activated and neutrophil extracellular traps were elevated in the plasma. IL-1β and soluble adhesion molecules may be the causal factors for neutrophil activation.

Macrophage biomimetic nanocarriers for anti-inflammation and targeted antiviral treatment in COVID-19

“…Patient serum is teeming with inflammatory mediators and cytokines, which could promote neutrophils activation and present a milieu favoring NETosis [ 40 ]. Indeed, under NETosis of neutrophils, NETs were released to form inflammation and microvascular thrombosis, which could exacerbate the CSS in COVID-19 patients [ 55 , 56 ]. Therefore, it would be an inspirational way for COVID-19 treatment if patient serums induced NETs could be suppressed.…”

“…In this study, PLGA@M manifested the talent in suppressing the formation of NETs induced by COVID-19 patient serum, suggesting that PLGA@M could play a multi-role in the treatment of COVID-19, and offer a comprehensive therapeutic benefit to patients. Meanwhile, NETs also engaged in the progression of multiple diseases including cardiovascular diseases [ 56 , 68 ], rheumatoid arthritis [ 69 ], diabetes [ 70 ], cancer [ 71 , 72 ] and so on, which meant that PLGA@M may have a potential to treat these diseases as well. However, the detailed mechanisms of how PLGA@M remove NETs and the possibility of clinical application still needed further exploration.…”

Anti-inflammatory effects of rosuvastatin treatment on coronary artery ectasia patients of different age groups

“…Elevated inflammatory markers, such as plasma IL-6 and plasma soluble adhesion molecules, are closely linked to the presence of coronary artery dilation [ 29 – 31 ]. One study has indicated increasing evidence that neutrophils and neutrophil-derived products participate in atherogenesis and CAE [ 32 ]. The neutrophil/lymphocyte ratio was higher in patients with CAD, coronary slow flow, and CAE than in those with a normal coronary anatomy.…”

Anti-inflammatory effects of rosuvastatin treatment in coronary artery ectasia patients in different age groups

“…Elevated in ammatory markers, such as plasma IL-6 and plasma soluble adhesion molecules, are closely linked to the presence of coronary artery dilation [22][23][24]. Some studies have indicated increasing evidence that neutrophils and neutrophil-derived products participate in atherogenesis and CAE [25]. The neutrophil/lymphocyte ratio was higher in patients with CAD, coronary slow ow and CAE than in individuals with normal coronary anatomy.…”