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|dc.identifier.citation||Reproductive Sciences, 2019; 26(3):1-13||en|
|dc.description.abstract||Glial adaptations within the central nervous system are well known to modulate central sensitization and pain. Recently, it has been suggested that activity of glial-related proinflammatory cytokines may potentiate peripheral inflammation, via central neurogenic processes. However, a role for altered glial function has not yet been investigated in the context of endometriosis, a chronic inflammatory condition in women associated with peripheral lesions, often manifesting with persistent pelvic pain. Using a minimally invasive mouse model of endometriosis, we investigated associations between peripheral endometriosis-like lesions and adaptations in central glial reactivity. Spinal cords (T13-S1) from female C57BL/6 mice with endometriosis-like lesions (ENDO) were imaged via fluorescent immunohistochemistry for the expression of glial fibrillary acidic protein (GFAP; astrocytes) and CD11b (microglia) in the dorsal horn (n = 5). Heightened variability ( P = .02) as well as an overall increase ( P = .04) in the mean area of GFAP immunoreactivity was found in ENDO versus saline-injected control animals. Interestingly, spinal levels showing the greatest alterations in GFAP immunoreactivity appeared to correlate with the spatial location of lesions within the abdominopelvic cavity. A subtle but significant increase in the mean area of CD11b immunostaining was also observed in ENDO mice compared to controls ( P = .02). This is the first study to describe adaptations in nonneuronal, immune-like cells of the central nervous system attributed to the presence of endometriosis-like lesions.||en|
|dc.description.statementofresponsibility||Kelsi N. Dodds, Elizabeth A. H. Beckett, Susan F. Evans, Mark R. Hutchinson||en|
|dc.rights||© The Author(s) 2018||en|
|dc.subject||endometriosis; glia; neurogenic inflammation; neuroimmune; pain||en|
|dc.title||Spinal glial adaptations occur in a minimally invasive mouse model of endometriosis: potential implications for lesion etiology and persistent pelvic pain||en|
|dc.identifier.orcid||Dodds, K. [0000-0003-0555-868X]||en|
|dc.identifier.orcid||Beckett, E. [0000-0001-8256-0375]||en|
|dc.identifier.orcid||Hutchinson, M. [0000-0003-2154-5950]||en|
|Appears in Collections:||Paediatrics publications|
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