Harnessing the inflammatory processes in endometriosis

The pathophysiology of endometriosis is underpinned by a complex interplay of inflammatory processes that are responsible for the local and systemic effects of the condition. Recent studies delve further into this inflammatory interplay; using animal models, they identify potential therapeutic tools and remind us to look beyond the endometriotic lesions. Key advances - In studies exploring the potential therapeutic value of a long-acting antibody directed against IL-8 (AMY109), the size of endometriotic lesions and extent of adhesions and fibrosis was reduced in a syngeneic model of endometriosis established in cynomolgus macaques3. - Researchers have suggested a mechanism by which Fusobacterium infection in the endometrium might be causative of endometriosis; pre-clinical studies using a syngeneic mouse model of endometriosis demonstrate that treatment with antibiotics reduces the severity of disease in Fusobacterium-infected animals7. - An increase in soma size was observed in the cortex, hippocampus, thalamus and hypothalamus of microglial cells in a mouse model of endometriosis; these results are suggestive of generalized glial cell activation and have ramifications for how we understand chronic pain and other neurological issues in endometriosis10. This is a preview of subscription content, access via your institution Access options Access Nature and 54 other Nature Portfolio journals Get Nature+, our best-value online-access subscription 27,99 € / 30 days cancel any time Subscribe to this journal Receive 12 print issues and online access 176,64 € per year only 14,72 € per issue Buy this article - Purchase on SpringerLink - Instant access to the full article PDF. 39,95 € Prices may be subject to local taxes which are calculated during checkout References Saunders, P. T. K. & Horne, A. W. Endometriosis: etiology, pathobiology, and therapeutic prospects. Cell 184, 2807–2824 (2021). Taylor, H. S., Kotlyar, A. M. & Flores, V. A. Endometriosis is a chronic systemic disease: clinical challenges and novel innovations. Lancet 397, 839–852 (2021). Nishimoto-Kakiuchi, A. et al. A long-acting anti-IL-8 antibody improves inflammation and fibrosis in endometriosis. Sci. Transl. Med. 15, eabq5858 (2023). Sikora, J., Smycz-Kubańska, M., Mielczarek-Palacz, A. & Kondera-Anasz, Z. Abnormal peritoneal regulation of chemokine activation–the role of IL-8 in pathogenesis of endometriosis. Am. J. Reprod. Immunol. 77, e12622 (2017). Klaus, T. & Deshmukh, S. pH-responsive antibodies for therapeutic applications. J. Biomed. Sci. 28, 11 (2021). American Society for Reproductive. Revised American Society for Reproductive Medicine classification of endometriosis: 1996. Fertil. Steril. 67, 817–821 (1997). Muraoka, A. et al. Fusobacterium infection facilitates the development of endometriosis through the phenotypic transition of endometrial fibroblasts. Sci. Transl. Med. 15, eadd1531 (2023). Uzuner, C., Mak, J., El-Assaad, F. & Condous, G. The bidirectional relationship between endometriosis and microbiome. Front. Endocrinol. 14, 1110824 (2023). Zhu, H. et al. Noteworthy perspectives on microglia in neuropsychiatric disorders. J. Neuroinflammation 20, 223 (2023). Bashir, S. T. et al. Endometriosis leads to central nervous system-wide glial activation in a mouse model of endometriosis. J. Neuroinflammation 20, 59 (2023). Author information Authors and Affiliations Corresponding author Ethics declarations Competing interests The author declares no competing interests. Rights and permissions About this article Cite this article Girling, J.E. Harnessing the inflammatory processes in endometriosis. Nat Rev Endocrinol 20, 69–70 (2024). https://doi.org/10.1038/s41574-023-00937-x Published: Version of record: Issue date: DOI: https://doi.org/10.1038/s41574-023-00937-x