AI Article Synopsis
- * Research indicates that endometriosis growth can occur even without ovarian steroid hormones, suggesting that the innate immune system also plays a role in its progression.
- * The article explores how bacterial endotoxin and TLR4 are involved in endometriosis and highlights their contribution to negative reproductive outcomes, particularly how increased macrophage presence in women with endometriosis affects the condition.
Article Abstract
Macrophages, dendritic cells, and Toll-like receptors (TLRs) are integral components of the innate immune system. This rapidly reactive system responds immediately to infectious or other non-self agents, thereby inducing an inflammatory response to protect the host until the activation of the slower adaptive immune system. The fundamentals of the innate immune system, functional characteristics of TLRs, and signaling pathways of TLR4 are discussed for the easy understanding by readers. Studies showed that the growth and progression of endometriosis continue even in ovariectomized animals. This indicates that besides ovarian steroid hormones, the growth of endometriosis can be regulated by the innate immune system in the pelvic environment. As a component of the innate immune system, increased infiltration of macrophages has been described in the intact tissue and peritoneal fluid of women with endometriosis. In this review article, we discuss the role of bacterial endotoxin and TLR4 in endometrium and endometriosis and outline the involvement of endotoxin in causing adverse reproductive outcome.
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| http://dx.doi.org/10.1159/000212061 | DOI Listing |
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