Low density neutrophils in patients with systemic lupus erythematosus, rheumatoid arthritis, and acute rheumatic fever

Abstract

Ficoll-Hypaque density gradient preparations of peripheral blood mononuclear cells from patients with systemic lupus erythematosus, rheumatoid arthritis, and acute rheumatic fever were highly "contaminated" with low buoyant density neutrophils. Plasma from these patients could induce an in vitro decrease of buoyancy in neutrophils with normal buoyant density. Similar change could be induced by complementactivated sera and aggregated gamma globulin. These data suggest that activated neutrophils are a common finding in the peripheral blood of these patients and may influence the interpretation of any studies with these cells. Functional studies of lymphocytes separated by Ficoll-Hypaque gradients should also take into account the higher degree of impurity of the cell preparations in patients with rheumatic diseases.Researchers have reported wide variations in the composition of mononuclear cell preparations obtained by Ficoll-Hypaque gradient preparations (1-3). The percentage of lymphocytes in the gradient-derived cell suspension is significantly decreased in patients with various forms of cancer (4-7). This decrease has been attributed to decreased buoyant density of the nonlymphoid cells in the peripheral blood of these patients, which causes a disproportionate number

A20-binding inhibitor of NF-κB (ABIN1) controls Toll-like receptor-mediated CCAAT/enhancer-binding protein β activation and protects from inflammatory disease

“…Also, as in patients with SLE and other chronic inflammatory conditions, peripheral blood and spleen contained a significant number of immature myeloid cells, characterized by low expression levels of Ly-6G (GR-1) and increased mRNA levels of neutrophil elastase (Ela2) and myeloperoxidase (Mpo) ( Fig. 2 G and H) (24,25). Lymph nodes and spleen were markedly increased in size and cellularity (Fig.…”

“…G-CSF is a major myeloid growth and survival factor (35), and myeloid expansion, including the appearance of increased numbers of macrophages and granulocytes, both in parenchymatous organs and peripheral blood, is a prominent phenotype of ABIN1-deficient mice. Notably, increased numbers of immature granulocytes also have been described in SLE patients (25,24), and two recent reports suggested granulocytes as key players in human SLE through a cell death-related release of DNA, which potently activates innate immune cells via TLR9 when complexed with other host cell-derived factors such as antibacterial peptides or autoreactive antibodies (4., 5,36,37). INOS regulates the production of cytotoxic NO, which are essential for defense against intracellular pathogens but also can promote host tissue damage if produced at exaggerated levels (38,39).…”

Identification of discrete tumor-induced myeloid-derived suppressor cell subpopulations with distinct T cell–suppressive activity

“…Up to now, such a low-density phenotype has been reported mainly for human granulocytes upon G-CSF treatment or fMLP activation and in patients confronted with overwhelming inflammation or cancer. [39][40][41] While in naive mice CD11b ϩ Ly6C ϩ Ly6G Ϫ splenocytes consisted mainly of monocytes and eosinophils; the latter did not expand in tumor-bearers. Furthermore, the phenotype of tumorinduced monocytes was not identical to that of their naive counterparts, expressing higher levels of CD71, CD115, and CD80.…”

High‐Dose, pulse intravenous methylprednisolone enhances fcγ receptor–mediated mononuclear phagocyte function in systemic lupus erythematosus

“…The percentage of positively stained cells within the mixed mononuclear cell preparation increased after the course of IVMP (pretreatment versus posttreatment 38 -t 15% versus 47 t 22%; P < 0.05). There was no significant contamination of the Ficoll-Hypaque mononuclear cell interface by neutrophils (33) and no change in the percentage of neutrophils present within the mononuclear cell preparation after IVMP (3 * 3% versus 6 -t 3%).…”