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 inhibition of cytotoxic T-cell function, cell division of T-lymphocytes, and the development of TH1 lymphocytes. Neurological effects
In response to physiologic and psychologic stress, prostaglandin E2 is involved in several inflammation and immunity pathways. As one of the most abundant prostaglandins in the body, Prostaglandin E2 is involved almost all typical inflammation markers such as redness, swelling, and pain. It regulates these responses through binding to G coupled protein prostaglandin E2 (PGE2) receptors (EP1, EP2, EP3, and EP4). The activation of these different EP receptors is dependent on the type of triggering stress stimuli and results in the corresponding stress response. Activation of EP1 via PGE2 results in the suppression of impulse behaviors in response to psychological stress. Prostaglandin E2 is involved in regulating illness induced memory impairment via activation of EP2. Prostaglandin E2 activation of EP3 results in regulation of illness induced fever. EP4 is functionally similar to EP2 and has also been shown in studies to have a role in hypothermia and anorexia.
Prostaglandins were discovered to be products of arachidonic acid and with the ability to radio label arachidonic acid in the early 1960s, American chemist E.J. Corey was able to synthesize prostaglandin E2 in the lab in the 1970. This advancement paved the way for later studies that helped define the actions and response of prostaglandin E2. Prostaglandin E2 was approved for medical use in the United States in 1977 and it is on the World Health Organizations List of Essential Medicines. Prostaglandin E2 was approved by the FDA in 1977. References
External links
"Dinoprostone". Drug Information Portal. U.S. National Library of Medicine.