Alpha‐7 nicotinic acetylcholine receptor (nAChR) agonist inhibits the development of endometriosis by regulating inflammation. (21st October 2016)

• Record Type: Journal Article
• Authors: Yamada‐Nomoto, Kaori; Yoshino, Osamu; Akiyama, Ikumi; Ushijima, Akemi; Ono, Yosuke; Shima, Tomoko; Nakashima, Akitoshi; Hayashi, Shusaku; Kadowaki, Makoto; Osuga, Yutaka; Saito, Shigeru
• Is Part Of: American journal of reproductive immunology. Volume 76:Number 6(2016)
• Page Start: 491
• Page End: 498
• Publication Date: 2016-10-21
• Subjects: endometriosis -- inflammation -- nicotine -- α‐7 nAChR; Human reproduction -- Immunological aspects -- Periodicals; 616.69206
• DOI: 10.1111/aji.12592
• Languages: English
• ISSNs: 1046-7408

Abstract

Abstract: Objective: We investigated α‐7 nAchR expression in human peritoneal macrophages and examined whether activation of nAchR might be a new therapy for endometriosis. Materials and methods: Human peritoneal fluid mononuclear cells (PFMC) were stimulated with lipopolysaccharide (LPS) in the presence of α‐7 nAChR agonists. In a murine endometriosis model, α‐7 nAChR modulators were administered. Results: Human PFMC expressed α‐7 nAChR at the mRNA and protein levels. Activation of α‐7 nAChR with its agonists led to significant ( P <.01) suppression of LPS‐induced interleukin (IL) ‐1β expression. In a murine endometriosis model, one week after inoculation of endometrium to the peritoneal cavity, α‐7 nAChR agonist significantly suppressed the expression of IL‐1β mRNA ( P <.01), which was negated when α‐7 nAChR antagonist was administered simultaneously. α‐7 nAChR agonist significantly suppressed the formation of endometriotic lesions, which was reversed with α‐7 nAChR antagonist. Conclusion: Activation of nAChR might be a new candidate for treatment of endometriosis.