been a report of oral PGE2 being used to treat ductus-dependent congenital heart diseases in newborns to delay surgical treatment until the pulmonary arteries grew. In addition, PGE2 was used in another report to dilate the ductus arteriosus in newborns with various cardiovascular defects to allow for better perfusion of the lungs and kidneys. On the other hand, the post-partal synthesis of PGE2 in newborns is considered one cause of patent ductus arteriosus. The aerosol form of PGE2 serves as a bronchodilator, but its use in this setting is limited by the fact that it also causes coughing. PGE2, similarly to PGE1, acts as a direct vasodilator by acting on smooth muscle to cause dilation of blood vessels. In addition, PGE2 inhibits platelet aggregation. PGE2 also suppresses T cell receptor signaling and proliferation, and may play a role in resolution of inflammation. In addition, PGE2 limits the immune response by preventing B-lymphocyte differentiation and their ability to present antigens. Central and peripheral nervous systems effects Prostaglandin E2 (PGE2) has a variety of functions within the central nervous system and peripheral nervous system. When PGE2 interacts with EP3 receptors, it increases body temperature, resulting in fever. PGE2 is also a predominant prostanoid that contributes to inflammation via enhancing edema and leukocyte infiltration from increased vascular permeability (allowing more blood flow into an inflamed area of the body) when acting on EP2 receptors. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) blocks the activity of COX-2, resulting in a decrease of PGE2 production. NSAIDs blocking COX-2 and decreasing the production of PGE2 remediates fever and inflammation. Additionally, PGE2 acting on EP1 and EP4 receptors are a component in feeling pain via inflammatory nociception. When PGE2 binds to EP1 and EP4 receptors, an increase in excitability via cation channels as well as inhibition of hyperpolarizing potassium (K+) channels, increase membrane excitability. As a result, this causes peripheral nerve endings to report painful stimuli. Immunity As mentioned previously, PGE2 contributes to the inflammation when bound to EP2 receptors. In terms of immunity, prostaglandins have the ability to regulate lymphocyte function. PGE2 affect T-lymphocyte formation by regulating apoptosis of immature thymocytes. In addition, it can suppress an immune response by inhibiting B lymphocytes from forming into antibody-secreting plasma cells. When this process is suppressed, it causes a decrease in a humoral antibody response because of the decrease in production of antibodies. PGE2 also has roles in