Pathogenesis of Endometriosis: Role of Macrophages in Endometriosis

In: Endometriosis and Adenomyosis · 2022 · pp. 57–74 · doi:10.1007/978-3-030-97236-3_5 · W4285144301
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Macrophages, regulated by toll-like receptor 4 and ovarian steroids, are central to endometriosis pathogenesis by mediating inflammation and promoting growth via hepatocyte growth factor.

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The paper reviews and synthesizes evidence on how pelvic inflammation, triggered by bacterial endotoxin (LPS) through toll-like receptor 4 (TLR4), contributes to endometriosis pathogenesis, emphasizing roles of innate immune activation. It reports that peritoneal macrophages retain estrogen and progesterone receptor encoding, and that ovarian steroids can cooperate with LPS to produce pelvic inflammatory responses that support development of endometriosis, with macrophage-driven and LPS-stimulated hepatocyte growth factor (HGF) acting as a growth-promoting factor. It also notes that treatment with the estrogen-suppressing agent GnRHa decreases local biological effects and tissue inflammation. This paper is centrally about endometriosis — it focuses on macrophages, LPS/TLR4-mediated inflammation, ovarian steroid signaling, and HGF in endometriosis pathogenesis.

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Abstract

Endometriosis is a chronic disease characterized by endometrial tissue located outside of the uterine cavity and is associated with chronic pelvic pain and infertility. However, an in-depth understanding of the pathophysiology of endometriosis is still elusive. It is generally believed that besides ovarian steroid hormones, the growth of endometriosis can be regulated by innate immune system in pelvic microenvironment by their interaction with endometrial cells and immune cells. We conducted a series of studies in perspectives of pelvic inflammation that is triggered primarily by bacterial endotoxin (lipopolysacccharide, LPS) and is mediated by toll-like receptor 4 (TLR4) and showed their involvement in the development of pelvic endometriosis. As a cellular component of innate immune system, macrophages (Mφ) play a central role in inducing pelvic inflammatory reaction. We further reported here that peritoneal Mφ retain receptors encoding for estrogen and progesterone and ovarian steroids also participate in producing an inflammatory response in pelvic cavity and involved in the growth of endometriosis either alone or in combination LPS. As a pleiotropic growth factor, Mφ-mediated and LPS-stimulated hepatocyte growth factor (HGF) plays significant growth promoting effect on endometriosis. Estrogen-suppressing agent, GnRHa, treatment exhibits local biological effect and is able to decrease tissue inflammation in endometriosis. We describe here the role Mφ and ovarian steroid hormones and orchestrated their involvement in the pathogenesis of endometriosis. Access this chapter Tax calculation will be finalised at checkout Purchases are for personal use only Similar content being viewed by others Change history 10 September 2022 Correction to:

References

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Author information Authors and Affiliations Corresponding author Editor information Editors and Affiliations Rights and permissions Copyright information © 2022 The Author(s), under exclusive license to Springer Nature Switzerland AG About this chapter Cite this chapter Khan, K.N. (2022). Pathogenesis of Endometriosis: Role of Macrophages in Endometriosis. In: Oral, E. (eds) Endometriosis and Adenomyosis. Springer, Cham. https://doi.org/10.1007/978-3-030-97236-3_5 Download citation DOI: https://doi.org/10.1007/978-3-030-97236-3_5 Published: Publisher Name: Springer, Cham Print ISBN: 978-3-030-97235-6 Online ISBN: 978-3-030-97236-3 eBook Packages: MedicineMedicine (R0)

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