TO THE QUESTION OF THE PATHOGENESIS OF SOME PRO-INFLAMMATORY AND IMMUNOLOGICAL LINKS OF THE ENDOMETRIOID DISEASE

Yulia Orlova
In: Bulletin of Problems Biology and Medicine · 2019 · vol. 4(1) , pp. 38 · doi:10.29254/2077-4214-2019-4-1-153-38-43 · W2996000933
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Abstract

The purpose of the literature review is to study the latest data on the pathogenetic links of chronic inflammation and disorders in the immune system in women with endometriosis. The diagnosis of endometriosis is now increasingly established in women of all ages. This trend has a poor prognosis, as already the total prevalence of endometrioid disease in women is 10%. It should be noted that the number of women of reproductive age with this pathology is increasing and according to various authors is in the range from 10 to 70%. Endometriosis poses a serious problem for normal functioning in various areas of the patient’s life and significantly impairs the quality of life. This is manifesting in the presence of pain, excessive menstrual bleeding and impaired reproductive potential, which is manifesting in primary and secondary infertility. However, in the presence of a wide variety of theories of the development of this pathology, including: implantation, genetic, hormonal, dysontogenetic, neoplastic, metaplastic, immune theories, etc., none of them fully describes the processes that lead to the development of endometriosis. However, many researchers recognize that endometriosis is a disease with aseptic chronic inflammation and significant impaired immune responses in these women. Implantation theory is that when the menstrual blood reverses through the fallopian tubes, the cells of the endometrium penetrate into the structures of the abdominal cavity due to their adhesive and invasive properties. However, retrograde menstruation is present in 90% of women, and endometriosis occurs in only 10% of women. Further, beyond the postulates of implantation theory, macrophages found in peritoneal fluid in 85% and in endometrial tissues of normal women increase in number and cause a whole pool of inflammatory reactions. Depending on the subspecies of M1 or M2 macrophages, they secrete a diverse number of cytokines and chemokines that, due to their functions, cause various processes in the abdomen and uterus. However, the role of the type of macrophage polarization in the genesis of endometrioid disease has not yet been fully identified, as some studies have shown an increase in the ratio of M2/M1 to M2 in endometrial cyst tissues and menstrual blood. In the endometrium of such women, the data regarding the type of polarization of macrophages differ. One source indicates a significant prevalence of M2 type, in others, the opposite of M1. Nowadays, it is known that chronic aseptic inflammation is maintained in endometrioid disease. Some literature data indicate that macrophage colony-stimulating factor (CSF-1) may be directly involved in this. It is responsible for the differentiation, proliferation and growth of macrophages. According to the literature, it is a predictor of oncogenicity in various gynecological diseases. CSF-1 increase in peritoneal fluid in women with endometriosis has also been observed. Breakdowns in the immune status, which is manifested not only in the altered immune response, but also in the evasion of endometrial cells by the destruction of NK cells eventually leads to impaired endometrial cells elimination processes and further disease progression. However, given that there are still unresolved questions about the direct involvement of macrophage polarization in the genesis of endometriosis and factors that contribute to the maintenance of chronic aseptic inflammation, this requires further study and detail to fully understand the pathogenetic patterns of endometrioid disease for implementation of necessary actions to improve diagnostic and treatment.

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