{"paper_id":"d90e517a-cf0d-48a5-bd8a-9e7f1dc5522d","body_text":"Abstract\nThe mechanisms that sustain endometrial tissues at ectopic sites in patients with endometriosis are poorly understood. It is well established now that endometriosis is associated with changes in population and functions of various leukocytes, including macrophages. Macrophages are the most abundant cells found in the peritoneal fluid and are the consistent feature of endometriotic lesion. They infiltrate endometriotic lesions where they undergo alternative activation as a consequence of signals generated within the invaded tissue. However, instead of clearing endometrial cells from the peritoneal cavity and restoring local homeostasis, macrophages appear to enhance their survival and proliferation by secreting growth, remodelling and inflammatory factors which could contribute to the development of endometriosis as well as to the disease-associated chronic pelvic inflammation and symptoms. Thus, unveiling the molecular mechanisms that underlie macrophage dysfunctions is a critical area of research, which would lead to the development of novel medical treatments for endometriosis. In this chapter, we described how macrophages can play a critical role in the pathophysiology of endometriosis not only via their weakened phagocytic functions but also via other major mechanisms revealed to date.\n*Author contributed equally with all other contributors.\nAccess this chapter\nTax calculation will be finalised at checkout\nPurchases are for personal use only\nSimilar content being viewed by others\nAbbreviations\n- CD:\n-\nCluster of differentiation\n- Cox-2:\n-\nCyclooxygenase-2\n- DCs:\n-\nDendritic cells\n- E2:\n-\nOestrogen\n- FGF:\n-\nFibroblast growth factor\n- ICAM-l:\n-\nIntercellular adhesion molecule-l\n- IL:\n-\nInterleukin\n- IFN-γ:\n-\nInterferon gamma\n- ISO-1:\n-\n((S,R) 3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic methyl ester\n- LFA-1:\n-\nLeukocyte function antigen-l\n- LPS:\n-\nLipopolysaccharide\n- MAPK:\n-\nMitogen-activated protein kinase\n- MCP-1:\n-\nMonocyte chemotactic protein-1\n- MIF:\n-\nMacrophage migration inhibitory factor\n- MMPs:\n-\nMatrix metalloproteinases\n- NF-κB:\n-\nNuclear factor kappa B\n- NGF:\n-\nNerve growth factor\n- NK:\n-\nNatural killer\n- PGE2:\n-\nProstaglandin-E2\n- PGF2α:\n-\nProstaglandin-F2α\n- PGs:\n-\nProstaglandins\n- PlGF:\n-\nPlacental growth factor\n- RANTES:\n-\nRegulated on activation, normal T cell expressed and secreted\n- StAR:\n-\nSteroidogenic acute regulatory protein\n- TGF:\n-\nTumour growth factor\n- TIMPs:\n-\nTissue inhibitors of MMPs\n- TNF-α:\n-\nTumour necrosis factor-alpha\n- uNK:\n-\nUterine natural killer\n- VEGF:\n-\nVascular endothelial growth factor\nReferences\nDmowski WP, Steele RW, Baker GF. 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Intraperitoneal recombinant gamma-interferon in patients with recurrent ascitic ovarian carcinoma: modulation of cytotoxicity and cytokine production in tumor-associated effectors and of major histocompatibility antigen expression on tumor cells. Cancer Res. 1990;50(22):7318–23.\nDuluc D, et al. Interferon-gamma reverses the immunosuppressive and protumoral properties and prevents the generation of human tumor-associated macrophages. Int J Cancer. 2009;125(2):367–73.\nAcknowledgement\nThis study is supported by CIHR grants MOP 93716, 120769 and 123259 to Pr. Ali Akoum, Chercheur National, FRQ-S.\nAuthor information\nAuthors and Affiliations\nCorresponding author\nEditor information\nEditors and Affiliations\nRights and permissions\nCopyright information\n© 2014 Springer Japan\nAbout this chapter\nCite this chapter\nAhmad, S.F., Michaud, N., Rakhila, H., Akoum, A. (2014). Macrophages in Pathophysiology of Endometriosis. In: Harada, T. (eds) Endometriosis. Springer, Tokyo. https://doi.org/10.1007/978-4-431-54421-0_6\nDownload citation\nDOI: https://doi.org/10.1007/978-4-431-54421-0_6\nPublished:\nPublisher Name: Springer, Tokyo\nPrint ISBN: 978-4-431-54420-3\nOnline ISBN: 978-4-431-54421-0\neBook Packages: MedicineMedicine (R0)","source_license":"CC0","license_restricted":false}