Estrogen could be responsible for endometriosis-associated chronic pain by activating macrophages — a type of immune cells — and nerve cells, which increases inflammation and sensitivity, a review study says.
The article “Villainous role of estrogen in macrophage-nerve interaction in endometriosis” was published in Reproductive Biology and Endocrinology.
Endometriosis is a chronic inflammatory disease whose specific causes are unknown. Its origin has been attributed to a combination of several factors. Recently, different circumstances affecting the progression of endometriosis and the relationship among them have been discovered.
Estrogen secretion is essential for disease progression, and the levels of this hormone are abnormally high in patients with endometriosis.
Researchers have found that the immune system also plays a role in this disease, increasing inflammation at the sites of injury. Additionally, the number of macrophages — the immune cells that contribute most to inflammation in the endometrium — is higher in endometriosis. This increase is thought to influence development of the disease and the frequency of endometriosis-related pain.
These findings also include the nervous system, as an abnormal distribution of nerve cells is common in endometriosis lesions, leading to an increase in nervous terminals and pain.
The review proposes that these three factors might be related and that this relationship might be the cause of endometriosis-related pain.
Estrogen can influence the action of various types of cells, as long as they express estrogen receptors. The macrophages and nerve cells on the endometrium express high amounts of estrogen receptors, which makes them more susceptible to this hormone.
The interaction of estrogen with estrogen receptors in the macrophages leads to activation and inflammatory response.
Activated macrophages produce nerve growth factors, molecules that cause the nerve cells to grow and form ramifications. This causes an increase in nerve terminals in the endometrium.
The inflammatory response lowers the threshold of the nerve cells, making them more sensitive. This combination of more sensitive cells and more nerve terminals leads to chronic pain.
Additionally, estrogen causes nerve cells to secrete migration factors that attract the macrophage to the site of injury, creating a vicious circle in which more inflammation creates more pain and the reaction to pain attracts macrophages that increase inflammation.
“The villainous communication between macrophages and nerve fibers has been demonstrated to be enhanced by the aberrant level of estrogen, providing a hypothesis in endometriosis-associated pain,” researchers wrote.
This suggests that “targeting estrogen levels [or] the receptors on macrophages and nerve fibers may be a potential approach to prevent the progression of endometriosis,” they added.
There are several substances that target hormone receptors and decrease hormonal level; such treatments might help prevent chronic pain in endometriosis patients.
However, ” a better understanding of estrogen in the interaction of nerves and macrophages inspires a novel insight of endometriosis-associated pain and provides a new strategy for diagnosis and a potentially valuable target for the treatment of endometriosis-associated pain,” researchers concluded.
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