Prostaglandin E2, Serum/Plasma | Healthmatters.io (2025)

Prostaglandin levels are a marker of inflammation and overall health.

Prostaglandins and thromboxane A2(TXA2), collectively termed prostanoids, are formed when arachidonic acid (AA), a 20-carbon unsaturated fatty acid, is released from the plasma membrane by phospholipases (PLAs) and metabolized by the sequential actions of prostaglandin G/H synthase, or cyclooxygenase (COX), and respective synthases.

When inflammation occurs in tissues, prostaglandin E2 (PGE2) is generated from arachidonic acid by the enzyme cyclooxygenase-2 (COX-2). PGE2 regulates multiple functions in various immune cells by binding to the downstream receptors EP1, EP2, EP3, and EP4.

There are four principal bioactive prostaglandins generatedin vivo: prostaglandin (PG) E2(PGE2), prostacyclin (PGI2), prostaglandin D2(PGD2) and prostaglandin F2α(PGF2α).They are ubiquitously produced – usually each cell type generates one or two dominant products - and act as autacrine and paracrine lipid mediators to maintain local homeostasis in the body. During an inflammatory response, both the level and the profile of prostaglandin production changes dramatically. Prostaglandin production is generally very low in uninflamed tissues, but increases immediately in acute inflammation prior to the recruitment of leukocytes and the infiltration of immune cells.

PGE2is one of the most abundant PGs produced in the body. Under physiological conditions, PGE2is an important mediator of many biological functions, such as regulation of immune responses, blood pressure, gastrointestinal integrity, and fertility.

Dysregulated PGE2synthesis or degradation has been associated with a wide range of pathological conditions.

In inflammation, PGE2is of particular interest because it is involved in all processes leading to the classic signs of inflammation: redness, swelling and pain.

Redness and edema result from increased blood flow into the inflamed tissue through PGE2-mediated augmentation of arterial dilatation and increased microvascular permeability. Pain results from the action of PGE2on peripheral sensory neurons and on central sites within the spinal cord and the brain.

PGE2, binding to different EP receptors, can regulate the function of many cell types including macrophages, dendritic cells and T and B lymphocytes leading to both pro- and anti-inflammatory effects. As pro-inflammatory mediator, PGE2contributes to the regulation of the cytokine expression profile of dendritic cells (DC)s and has been reported to bias T cell differentiation towards a T helper (Th) 1 or Th2 response.

PGE2can thus modulate various steps of inflammation in a context-dependent manner and coordinate the whole process in both pro-inflammatory and anti-inflammatory directions. This dual role of PGE2and its receptors in modulating the inflammatory response has been observed in several disorders. In atherosclerosis, EP4 deficiency promotes macrophage apoptosis and suppresses early atherosclerosis in LDLR−/−mice chimeric for EP4−/−in hematopoietic cells after 8 weeks on a Western diet. EP2 deficiency in hematopoietic cells revealed a trend for similar, but modest, effects on atherosclerosis.

References:

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