Abstract
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.
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 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 -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.