Eicosanoids are rapidly metabolized to inactive products and therefore are short-lived. Accordingly, the eicosanoid-receptor interaction is typically limited to a local interaction: cells, upon stimulation, metabolize arachidonic acid to an eicosanoid which then binds cognate receptors on either its parent cell (acting as an Autocrine signalling molecule) or on nearby cells (acting as a Paracrine signalling molecule) to trigger functional responses within a restricted tissue area, e.g. an inflammatory response to an invading pathogen.
Eicosanoids are swiftly broken down into inactive components and thus have a short lifespan. Consequently, the eicosanoid-receptor interaction is usually confined to a localized engagement: cells, upon stimulation, convert arachidonic acid into an eicosanoid that then binds to cognate receptors on either its parent cell (acting as an Autocrine signaling molecule) or nearby cells (acting as a Paracrine signaling molecule) to initiate functional responses within a limited tissue region, such as an immune response against an invading pathogen.