Toll-like receptors in innate immunity: role of bacterial endotoxin and toll-like receptor 4 in endometrium and endometriosis.
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.
Department of Obstetrics and Gynecology, Nagasaki University Graduate School of Biomedical Sciences, Sakamoto, Nagasaki, Japan. nemokhan@nagasaki-u.ac.jp
Khaleque Newaz
KN
Khan
Michio
M
Kitajima
Koichi
K
Hiraki
Akira
A
Fujishita
Ichiro
I
Sekine
Tadayuki
T
Ishimaru
Hideaki
H
Masuzaki
D000818:Animals; D004715:Endometriosis / Q000276:immunology*; D004717:Endometrium / Q000276:immunology* / Q000378:metabolism; D004731:Endotoxins / Q000009:adverse effects*; D005260:Female; D006801:Humans; D007113:Immunity, Innate; D008264:Macrophages / Q000502:physiology; D015398:Signal Transduction / Q000276:immunology; D051197:Toll-Like Receptor 4 / Q000276:immunology* / Q000378:metabolism
D004731:Endotoxins; D051197:Toll-Like Receptor 4