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Showing posts with the label cox-1

Inflammation, NSAIDs, Painkillers, Immunity system

Inflammation  is t he reaction of a part of the body to injury or infection, characterized by swelling, heat, redness, and pain. The process includes increased blood flow with an influx of white blood cells and other chemical substances that facilitate healing. Cyclooxygenase  (COX), officially known as prostaglandin-endoperoxide synthase (PTGS), is an enzyme (specifically, a family of isozymes, EC 1.14.99.1) that is responsible for formation of prostanoids, including thromboxane and prostaglandins such as prostacyclin. The  prostaglandins  (PG) are a group of physiologically active lipid compounds having diverse hormone-like effects in animals. Q: Why does your body temperature rise when you have the flu? A : " Your body temperature rises when you have the flu as a way of fighting off the influenza virus; viruses thrive best at 98.6 degrees Fahrenheit—normal body temperature. When your body is hotter it's harder for the flu virus to survive. A...

Ibuprofen and other widely used non-steroidal anti-inflammatory drugs inhibit antibody production in human cells

Abstract The widely used non-steroidal anti-inflammatory drugs (NSAIDs) function mainly through inhibition of cyclooxygenases 1 and 2 (Cox-1 and Cox-2). Unlike Cox-1, Cox-2 is considered an inducible and pro-inflammatory enzyme. We previously reported that Cox-2 is upregulated in activated human B lymphocytes and using Cox-2 selective inhibitors that Cox-2 is required for optimal antibody synthesis. It is not known whether commonly used non-prescription and non-Cox-2 selective drugs also influence antibody synthesis. Herein, we tested a variety of Cox-1/Cox-2 non-selective NSAIDs, namely ibuprofen, tylenol, aspirin and naproxen and report that they blunt IgM and IgG synthesis in stimulated human peripheral blood mononuclear cells (PBMC). Ibuprofen had its most profound effects in inhibiting human PBMCs and purified B lymphocyte IgM and IgG synthesis when administered in the first few days after activation. As shown by viability assays, ibuprofen did not kill B cells. The implication...