Both primary infection and accumulation of cellular debris initiate the stress response of the endoplasmic reticulum and increase the regulation of inflammatory enzymes, including microsomal prostaglandin E synthase-1 (mPGES-1) and prostaglandin-endoperoxide synthase 2 (also known such as COX-2), which subsequently produce eicosanoids: prostaglandins (PG), leukotrienes (LT) and thromboxanes (TX). The gene discussed is PTGS2; the disease is infection.