Spinal glial adaptations occur in a minimally invasive mouse model of endometriosis: potential implications for lesion etiology and persistent pelvic pain
dc.contributor.author | Dodds, K. | |
dc.contributor.author | Beckett, E. | |
dc.contributor.author | Evans, S. | |
dc.contributor.author | Hutchinson, M. | |
dc.date.issued | 2019 | |
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. | |
dc.description.statementofresponsibility | Kelsi N. Dodds, Elizabeth A. H. Beckett, Susan F. Evans, Mark R. Hutchinson | |
dc.identifier.citation | Reproductive Sciences, 2019; 26(3):1-13 | |
dc.identifier.doi | 10.1177/1933719118773405 | |
dc.identifier.issn | 1556-7117 | |
dc.identifier.issn | 1933-7205 | |
dc.identifier.orcid | Dodds, K. [0000-0003-0555-868X] | |
dc.identifier.orcid | Beckett, E. [0000-0001-8256-0375] | |
dc.identifier.orcid | Evans, S. [0000-0003-0347-604X] | |
dc.identifier.orcid | Hutchinson, M. [0000-0003-2154-5950] | |
dc.identifier.uri | http://hdl.handle.net/2440/118313 | |
dc.language.iso | en | |
dc.publisher | Elsevier | |
dc.relation.grant | http://purl.org/au-research/grants/arc/DP110100297 | |
dc.rights | © The Author(s) 2018 | |
dc.source.uri | https://doi.org/10.1177/1933719118773405 | |
dc.subject | endometriosis | |
dc.subject | glia | |
dc.subject | neurogenic inflammation | |
dc.subject | neuroimmune | |
dc.subject | pain | |
dc.title | Spinal glial adaptations occur in a minimally invasive mouse model of endometriosis: potential implications for lesion etiology and persistent pelvic pain | |
dc.type | Journal article | |
pubs.publication-status | Published |