Authors
Kiara Wiggins, Zena Del Mundo, Julio Ayala Angulo, Nandini Naidu, Angelina Saba, Lily Zhou, Christopher Garcia, Christy M Nguyen, Naveena Ujagar, Jamie-Jean De La Torre, Gabriela De Robles, Angie Rivera, Davina Trinh, Roberto Tinoco, Alexander S Kauffman, Varykina G Thackray, Anshu Agrawal, Marcus Seldin, Gabriela Pacheco-Sanchez, Dequina A Nicholas
Published in
Reproduction (Cambridge, England). Jul 01, 2026. Epub Jul 01, 2026.
Abstract
Polyendocrine metabolic ovarian syndrome (PMOS), formerly termed polycystic ovary syndrome (PCOS), is a reproductive disorder with heterogeneous symptoms and severity. Despite extensive research documenting chronic immune dysfunction as a hallmark of PMOS, the specific mechanisms of immune activation remain poorly understood. Emerging evidence suggests that gut-derived bacterial endotoxins, particularly lipopolysaccharide (LPS), can breach intestinal barriers and trigger systemic inflammation via Toll-like receptor 4 (TLR4). This study examined the role of TLR4 in PMOS-like pathology using a letrozole (LET)-induced mouse model. In LET-treated wild-type female mice, serum LPS and its carrier protein LBP were elevated compared to LET-treated TLR4-/- mice. Additionally, TLR4 deficiency attenuated multiple PMOS-like features, including elevated luteinizing hormone, anovulation, and metabolic dysfunction. LET-treated TLR4-/- mice also preserved estrous cycling and fertility, maintained gut barrier integrity, and reduced inflammatory markers. These findings support TLR4 as an important contributor to multiple features of PMOS-like pathology. This novel work highlights TLR4-mediated inflammation as a potential target for anti-inflammatory treatments in women with PMOS.
PMID:
42384365
Bibliographic data and abstract were imported from PubMed on 01 Jul 2026.
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