Peer-reviewed veterinary case report
Expression of indoleamine 2,3-dioxygenase 1 as transcript and protein in the healthy and diseased equine endometrium.
- Journal:
- Research in veterinary science
- Year:
- 2018
- Authors:
- Schöniger, Sandra et al.
- Affiliation:
- Institute of Pathology · Germany
- Species:
- horse
Abstract
The enzyme indoleamine 2,3-dioxygenase 1 (IDO1) acts immunomodulatory and restricts bacterial growth. In the uterus of women and mice, it likely contributes to tissue homeostasis and disease pathogenesis. Pregnancy failure in mares is often caused by endometritis and endometrosis. The pathogenesis of nonsuppurative endometritis and endometrosis is still uncertain. To the authors' knowledge, no information on IDO1 expression in the equine endometrium is published. Aim of this study was to examine the presence of IDO1 as transcripts and proteins in the healthy and diseased endometrium of 25 mares and to determine its cellular expression. By PCR, IDO1 transcripts were detected in healthy (3 mares) and diseased endometria (22 mares). Western blot on 15 samples showed the concurrent presence of IDO1 proteins. Immunohistochemistry revealed its expression in macrophages and epithelial cells. Endometria of 21 mares showed an intense staining of glandular epithelia, whereas glands of the remaining 4 mares were negative or contained only few positive cells. Tissue samples of all mares showed a minimal to mild IDO1 expression in the surface epithelium and glandular ducts. Quantification of immunohistochemistry on biopsies of 6 mares collected at different stages of the same endometrial cycle indicated that the IDO1 expression is not influenced by the endometrial cycle. This study confirmed IDO1 expression also in the equine endometrium and suggests an immunomodulatory role of uterine macrophages and epithelial cells. A markedly reduced glandular IDO1 expression as detected in 4 mares may be associated with alterations of uterine immune defenses.
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Search related cases →Original publication: https://pubmed.ncbi.nlm.nih.gov/29547726/