Niclosamide suppresses macrophage-induced inflammation in endometriosis†

Nikola Sekulovski, Allison E Whorton, Tomoki Tanaka, Yasushi Hirota, Mingxin Shi, James A MacLean, Julio Ricardo Loret de Mola, Kathleen Groesch, Paula Diaz-Sylvester, Paula Díaz‐Sylvester, Teresa Wilson, Kanako Hayashi
Biology of reproduction · 2020 · vol. 102(5) , pp. 1011–1019 · doi:10.1093/biolre/ioaa010 · PMID:31950153 · W2998799901
article OA: bronze CC0 ⤵ 14 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Niclosamide inhibited macrophage-induced proliferation and pro-inflammatory cytokine/chemokine secretion in human endometriotic stromal cells by suppressing STAT3 and NFκB signaling.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

Endometriosis is a common gynecological disease, which causes chronic pelvic pain and infertility in women of reproductive age. Due to limited efficacy of current treatment options, a critical need exists to develop new and effective treatments for endometriosis. Niclosamide is an efficacious and FDA-approved drug for the treatment of helminthosis in humans that has been used for decades. We have reported that niclosamide reduces growth and progression of endometriosis-like lesions via targeting STAT3 and NFĸB signaling in a mouse model of endometriosis. To examine the effects of niclosamide on macrophage-induced inflammation in endometriosis, a total of 29 stage III-IV endometrioma samples were used to isolate human endometriotic stromal cells (hESCs). M1 or M2 macrophages were isolated and differentiated from fresh human peripheral blood samples. Then, hESCs were cultured in conditioned media (CM) from macrophages with/without niclosamide. Niclosamide dose dependently reduced cell viability and the activity of STAT3 and NFκB signaling in hESCs. While macrophage CM stimulated cell viability in hESCs, niclosamide inhibited this stimulation. Macrophage CM stimulated the secretion of proinflammatory cytokines and chemokines from hESCs. Most of these secreted factors were inhibited by niclosamide. These results indicate that niclosamide is able to reduce macrophage-induced cell viability and cytokine/chemokine secretion in hESCs by inhibiting inflammatory mechanisms via STAT3 and/or NFκB signaling.

My notes (saved in your browser only)

Condition tags

mesh:D004715endometriosisendometriomachronic_pelvic_paininfertility

MeSH descriptors

Cell Survival Endometriosis Macrophages Macrophages Niclosamide Animals Anticestodal Agents Anticestodal Agents Cells, Cultured Cell Survival Endometriosis Endometriosis Female Gene Expression Regulation Gene Expression Regulation Humans Inflammation Inflammation Macrophages Mice

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (90)

Cited by (14)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-04T00:00:01.174412+00:00
pubmed
last seen: 2026-05-13T22:22:17.025735+00:00
License: CC0 · commercial use OK