Efficacy of niclosamide on the intra‐abdominal inflammatory environment in endometriosis

Mingxin Shi, Nikola Sekulovski, Allison E Whorton, James A. MacLean, Erin Greaves, Kanako Hayashi
FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021 · vol. 35(5) , pp. e21584 · doi:10.1096/fj.202002541rrr · PMID:33860549 · W3154765574
article OA: green CC0 ⤵ 8 in-corpus citations
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Niclosamide reduced GATA6-expressing large peritoneal macrophages, associated inflammation, and nerve growth in an endometriosis mouse model, suggesting its potential as a non-hormonal therapy.

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Abstract

Endometriosis, a common gynecological disease, causes chronic pelvic pain and infertility in women of reproductive age. Due to the limited efficacy of current therapies, a critical need exists to develop new treatments for endometriosis. Inflammatory dysfunction, instigated by abnormal macrophage (MΦ) function, contributes to disease development and progression. However, the fundamental role of the heterogeneous population of peritoneal MΦ and their potential druggable functions is uncertain. Here we report that GATA6-expressing large peritoneal MΦ (LPM) were increased in the peritoneal cavity following lesion induction. This was associated with increased cytokine and chemokine secretion in the peritoneal fluid (PF), as well as MΦ infiltration, vascularization and innervation in endometriosis-like lesions (ELL). Niclosamide, an FDA-approved anti-helminthic drug, was effective in reducing LPM number, but not small peritoneal MΦ (SPM), in the PF. Niclosamide also inhibits aberrant inflammation in the PF, ELL, pelvic organs (uterus and vagina) and dorsal root ganglion (DRG), as well as MΦ infiltration, vascularization and innervation in the ELL. PF from ELL mice stimulated DRG outgrowth in vitro, whereas the PF from niclosamide-treated ELL mice lacked the strong stimulatory nerve growth response. These results suggest LPM induce aberrant inflammation in endometriosis promoting lesion progression and establishment of the inflammatory environment that sensitizes peripheral nociceptors in the lesions and other pelvic organs, leading to increased hyperalgesia. Our findings provide the rationale for targeting LPM and their functions with niclosamide and its efficacy in endometriosis as a new non-hormonal therapy to reduce aberrant inflammation which may ultimately diminish associated pain.

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Condition tags

mesh:D004715endometriosischronic_pelvic_paininfertility

MeSH descriptors

Anticestodal Agents Endometriosis Ganglia, Spinal GATA6 Transcription Factor Inflammation Macrophages, Peritoneal Niclosamide Animals Anticestodal Agents Endometriosis Female Ganglia, Spinal Ganglia, Spinal GATA6 Transcription Factor GATA6 Transcription Factor Inflammation Inflammation Inflammation Macrophages, Peritoneal Macrophages, Peritoneal

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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.

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