Abstract
BackgroundNET (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.ResultsThe 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.ConclusionThe 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.
Highlights
neutrophil extracellular traps (NETs) has been shown to directly influence inflammation; in Systemic Lupus Erythematosus (SLE), it is reportedly a plausible cause for the broken self-tolerance that contributes to this pathology
Patients and controls Seventeen patients who fulfilled the American College of Rheumatology (ACR) classification criteria for SLE [16] and registered at a lupus clinic affiliated with Isafahan University of Medical Sciences, and 17 healthy volunteers were enrolled in this study (Supplementary Document 1, Table S1)
NET visualization, collection and comparison After PMA (Phorbol 12-myristate 13-acetate) stimulation, the production of NET from the neutrophils was confirmed with the observation of the filamentous appearance of unwound chromatin, which coexisted with neutrophil elastase (NE) (Fig. 1)
Summary
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. The effects induced by NET on neutrophils help prolong inflammation; the NET collected from SLE patients is stronger than the NET from healthy individuals
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
