The impact of neutrophil extracellular trap from patients with systemic lupus erythematosus on the viability, CD11b expression and oxidative burst of healthy neutrophils

• Published in: BMC immunology Vol. 22; no. 1; p. 12
• Main Authors: Fatemi, Alimohammad, Alipour, Razieh, Khanahmad, Hossein, Alsahebfosul, Fereshteh, Andalib, Alireza, Pourazar, Abbasali
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 05-02-2021; BioMed Central; BMC
• Subjects: Apoptosis; CD11b antigen; Cell death; Chronic illnesses; Damage-associated molecular patterns (DAMP); Development and progression; DNA; Granulocytes; Health aspects; Immune response; Immunological tolerance; Inflammation; Integrins; Leukocytes (neutrophilic); Lupus; Medical research; Neutrophil extracellular trap (NET); Neutrophils; Oxidative stress; Pathogenesis; Physiological aspects; Production increases; Self; Systemic lupus erythematosus; Systemic lupus erythematosus (SLE); Viability; Iran; Damage-associated molecular patterns (DAMP); Inflammation; Systemic lupus erythematosus (SLE); Neutrophil extracellular trap (NET); Neutrophils
• ISSN: 1471-2172; 1471-2172
• DOI: 10.1186/s12865-021-00402-2

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.
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.
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.