Alimohammad Fatemi1, Razieh Alipour2, Hossein Khanahmad3, Fereshteh Alsahebfosul2, Alireza Andalib2, Abbasali Pourazar4. 1. Department of Internal Medicine, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. 2. Department of Immunology, Medical School, Isfahan University of Medical Sciences, Hezar Jerib Street, Isfahan, IR, 81746-73695, Iran. 3. Department of Genetics and Molecular Biology, School of Medicine, Pediatric Inherited Diseases Research Center, Research Institute for Primordial Prevention of Non-communicable Disease, Isfahan University of Medical Sciences, Isfahan, Iran. 4. Department of Immunology, Medical School, Isfahan University of Medical Sciences, Hezar Jerib Street, Isfahan, IR, 81746-73695, Iran. pourazar@med.mui.ac.ir.
Abstract
BACKGROUND: NET (neutrophil extracellular trap) has been shown to directly influence inflammation; in SLE (systemic lupus erythematosus), it is reportedly a plausible cause for the broken self-tolerance that contributes to this pathology. Meanwhile, the role of NET is not easily explicable, and there is a serious discrepancy in the role of NET in SLE pathology and generally inflammation; in particular, the interactions of neutrophils with NET have been rarely inspected. This study evaluates the effect of NET on neutrophils in the context of SLE. The neutrophils were incubated by the collected NET (from SLE patients and healthy controls) and their expression of an activation marker, viability and oxidative burst ability were measured. RESULTS: The level of cell mortality, CD11b expression and the oxidative burst capacity were elevated in NET-treated neutrophils. Also, the elevation caused by the SLE NET was higher than that produced by the healthy NET. CONCLUSION: The decreased neutrophil viability was not due to the increase in apoptosis; rather, it was because of the augmentation of other inflammatory cell-death modes. The upregulation of CD11b implies that NET causes neutrophils to more actively contribute to inflammation. The increased oxidative burst capacity of neutrophils can play a double role in inflammation. Overall, the effects induced by NET on neutrophils help prolong inflammation; accordingly, the NET collected from SLE patients is stronger than the NET from healthy individuals.
BACKGROUND: NET (neutrophil extracellular trap) has been shown to directly influence inflammation; in SLE (systemic lupus erythematosus), it is reportedly a plausible cause for the broken self-tolerance that contributes to this pathology. Meanwhile, the role of NET is not easily explicable, and there is a serious discrepancy in the role of NET in SLE pathology and generally inflammation; in particular, the interactions of neutrophils with NET have been rarely inspected. This study evaluates the effect of NET on neutrophils in the context of SLE. The neutrophils were incubated by the collected NET (from SLE patients and healthy controls) and their expression of an activation marker, viability and oxidative burst ability were measured. RESULTS: The level of cell mortality, CD11b expression and the oxidative burst capacity were elevated in NET-treated neutrophils. Also, the elevation caused by the SLE NET was higher than that produced by the healthy NET. CONCLUSION: The decreased neutrophil viability was not due to the increase in apoptosis; rather, it was because of the augmentation of other inflammatory cell-death modes. The upregulation of CD11b implies that NET causes neutrophils to more actively contribute to inflammation. The increased oxidative burst capacity of neutrophils can play a double role in inflammation. Overall, the effects induced by NET on neutrophils help prolong inflammation; accordingly, the NET collected from SLE patients is stronger than the NET from healthy individuals.
Authors: J Xu; Y Jiang; J Wang; X Shi; Q Liu; Z Liu; Y Li; M J Scott; G Xiao; S Li; L Fan; T R Billiar; M A Wilson; J Fan Journal: Cell Death Differ Date: 2014-04-25 Impact factor: 15.828
Authors: Maurizio Bruschi; Andrea Petretto; Laura Santucci; Augusto Vaglio; Federico Pratesi; Paola Migliorini; Roberta Bertelli; Chiara Lavarello; Martina Bartolucci; Giovanni Candiano; Marco Prunotto; Gian Marco Ghiggeri Journal: Sci Rep Date: 2019-05-28 Impact factor: 4.379