International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2026
Regulatory role of the soluble TLR4 form in HMGB1-driven inflammation in PCOS: Integration of biochemical and molecular docking evidence.
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Atheeb Ahmed Kareem, Hussein Saba Zuhair
Аннотация
OBJECTIVE: Given the recognized role of chronic low-grade inflammation in polycystic ovary syndrome (PCOS), the aim of the present study was to investigate the role of the serum high-mobility group box 1 (HMGB1)-Toll-like receptor 4 (TLR4)-interferon beta (IFN-β) signaling axis and its association with immune-metabolic dysfunctions in women with PCOS.
METHODS: This was a case-control study involving 90 Iraqi women aged 18-45 years, including 50 newly diagnosed PCOS patients and 40 healthy controls. Serum levels of HMGB1, soluble Toll-like receptor 4 (sTLR4), and INF-β were measured using enzyme-linked immunosorbent assay (ELISA). An automated analyzer was employed to assess the hormonal profile. Molecular docking simulations were performed using MOE software to evaluate the interaction of HMGB1 with both membrane-bond TLR4 and its soluble form.
RESULTS: The PCOS group exhibited significant alterations in hormonal profiles compared to healthy controls. Serum levels of HMGB1, sTLR4, and INF-β were significantly elevated, consistent with a state of low-grade inflammation. Molecular docking analysis demonstrated favorable binding of HMGB1 to both TLR4 and sTLR4, with a slightly stronger affinity for sTLR4 (-7.20 kcal/mol; RMSD 2.13 Å) than TLR4 (-6.23 kcal/mol; RMSD 1.73 Å).
CONCLUSION: The HMGB1-TLR4-INF-β signaling axis appears to contribute to low-grade inflammation in PCOS. The soluble form of TLR4 may act as a regulatory modulator that attenuates inflammatory signaling. The integration of biochemical and computational data findings provides novel insights into immune-metabolic dysregulation in PCOS and highlights potential therapeutic targets for modulating inflammation.
METHODS: This was a case-control study involving 90 Iraqi women aged 18-45 years, including 50 newly diagnosed PCOS patients and 40 healthy controls. Serum levels of HMGB1, soluble Toll-like receptor 4 (sTLR4), and INF-β were measured using enzyme-linked immunosorbent assay (ELISA). An automated analyzer was employed to assess the hormonal profile. Molecular docking simulations were performed using MOE software to evaluate the interaction of HMGB1 with both membrane-bond TLR4 and its soluble form.
RESULTS: The PCOS group exhibited significant alterations in hormonal profiles compared to healthy controls. Serum levels of HMGB1, sTLR4, and INF-β were significantly elevated, consistent with a state of low-grade inflammation. Molecular docking analysis demonstrated favorable binding of HMGB1 to both TLR4 and sTLR4, with a slightly stronger affinity for sTLR4 (-7.20 kcal/mol; RMSD 2.13 Å) than TLR4 (-6.23 kcal/mol; RMSD 1.73 Å).
CONCLUSION: The HMGB1-TLR4-INF-β signaling axis appears to contribute to low-grade inflammation in PCOS. The soluble form of TLR4 may act as a regulatory modulator that attenuates inflammatory signaling. The integration of biochemical and computational data findings provides novel insights into immune-metabolic dysregulation in PCOS and highlights potential therapeutic targets for modulating inflammation.