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Lupus Neutrophil Extracellular Traps Render High Density Lipoprotein Oxidized and Proatherogenic

Cardiovascular risk is significantly increased in systemic lupus erythematosus (SLE) patients. This phenomenon cannot be explained by the Framingham risk equation.  Previous reports suggest that high density lipoprotein (HDL) becomes oxidized in autoimmune diseases such as rheumatoid arthritis and SLE. We previously demonstrated that phagocyte-derived myeloperoxidase (MPO) oxidizes HDL and renders the lipoprotein atherogenic by impairing reverse cholesterol transport. Neutrophil extracellular traps (NETs) are an innate antimicrobial mechanism wherein granulocytes extrude their chromatin and antimicrobial peptides, including MPO. Nitric oxide synthase (NOS) is also capable of generating the reactive nitrogen species required for HDL oxidation and is highly present in neutrophils. As a subset of lupus granulocytes termed low density granulocytes (LDGs) display an enhanced capacity to form NETs, we hypothesized that the MPO and NOS present in these structures may represent sources of HDL oxidation, thereby leading to vascular damage and acceleration of atherogenesis.

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Source: American College of Rheumatology/ACR Annual Meeting


Lupus Neutrophil Extracellular Traps Render High Density Lipoprotein Oxidized and Proatherogenic

Cardiovascular risk is significantly increased in systemic lupus erythematosus (SLE) patients. This phenomenon cannot be explained by the Framingham risk equation.  Previous reports suggest that high density lipoprotein (HDL) becomes oxidized in autoimmune diseases such as rheumatoid arthritis and SLE. We previously demonstrated that phagocyte-derived myeloperoxidase (MPO) oxidizes HDL and renders the lipoprotein atherogenic by impairing reverse cholesterol transport. Neutrophil extracellular traps (NETs) are an innate antimicrobial mechanism wherein granulocytes extrude their chromatin and antimicrobial peptides, including MPO. Nitric oxide synthase (NOS) is also capable of generating the reactive nitrogen species required for HDL oxidation and is highly present in neutrophils. As a subset of lupus granulocytes termed low density granulocytes (LDGs) display an enhanced capacity to form NETs, we hypothesized that the MPO and NOS present in these structures may represent sources of HDL oxidation, thereby leading to vascular damage and acceleration of atherogenesis.

***

Click here to read full article.

Source: American College of Rheumatology/ACR Annual Meeting



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