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
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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.
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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.
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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.
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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
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DOI: https://doi.org/10.1038/s41574-023-00937-x
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