Inflammation is a multi-faceted primarily cellular response to injury. After an inflammatory stimulus, neutrophils are activated and migrate to the source of the insult. Neutrophils release a number of substances, including digestive enzymes and inflammatory mediators. Some of these mediators result in arachidonic acid metabolism, which is further converted by cyclooxygenase (COX) and lipoxygenase (LOX) into inflammatory prostaglandins and other components. This results in inflammation and ultimately discomfort.  

      What Role do Cytokines and Neutrophils play in INFLAMMATION?

Inflammation is triggered by chemical mediators (histamine, serotonin, etc.) and mediators from white blood cells, especially neutrophils (prostaglandins, leukotrienes, lysosomal enzymes, etc.). Injured cells produce cytokines such as IL-1ß and TNFa that stimulate the emigration of neutrophils from the capillaries so they release their destructive enzymes at the site of inflammation. The initiating cause of inflammation does not determine the results at the cellular and tissue level. In all cases of inflammation, neutrophils are attracted to the site of injury and invade the tissue, and amplify the inflammatory cascade.