Analysis of activated neutrophils Ly6G+CD11b+ and low density granulocytes CD15+CD14low and the plasmatic concentration of IL-18 in mice with pristane-induced systemic lupus erythematosus (SLE).

Abstract

Systemic Lupus Erythematosus (SLE) is an auto immune disease that has a complex etiology involving environmental, genetic and hormonal factors and is characterized by loss of immunologic auto-tolerance, activation and proliferation of auto-reactive T cells and production of auto-antibodies. Although the specific role of neutrophils in SLE remains unknown, the increased production of auto-antigens and, thus, of auto-antibodies seems to be correlated with the release of neutrophil extracellular traps (NET), a form of cell death exclusive to neutrophils. Patients with SLE, have increased numbers of peripheral neutrophils and higher expression of CD11b (activated neutrophil marker) which is related to clinical activity. Low density granulocytes (LDG) are prone to release of NETs and are higher levels in sera from lupus patients. Experimental models, including pristane induced lupus, develop syndromes similar to human SLE. The administration of pristane in Balb/c mice induces inflammatory responses and auto-antibody production, reproducing serological, histopathological and clinical factors of lupus. We aim to evaluate in this model the presence of activated neutrophils Ly6G+CD11b+ and LDGs CD15+CD14low in peripheral blood, peritoneal wash and spleen, and the production of plasmatic IL-18, in order to evaluate some aspects of the inflammatory process in lupus. (AU)