1. Inflammatory Cells in Control and Prolapsed Uterosacral Ligament Tissue.
- Author
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Orlicky DJ, Smith EE, Johnson J, Hilton AE, Guess MK, Rascoff LG, Arruda JS, Hutchinson-Colas JA, Yang I, and Connell KA
- Subjects
- Female, Humans, Middle Aged, Uterus pathology, Uterus metabolism, Macrophages pathology, Macrophages metabolism, Inflammation pathology, Inflammation metabolism, Aged, Neutrophils metabolism, Neutrophils pathology, Adult, Ligaments pathology, Pelvic Organ Prolapse pathology, Pelvic Organ Prolapse metabolism, Pelvic Organ Prolapse etiology, Mast Cells pathology, Mast Cells metabolism
- Abstract
Pelvic organ prolapse (POP), a downward descent of the vagina and/or uterus through the vaginal canal, is a prevalent condition affecting up to 40% of women. Several risk factors of POP have been identified, including childbirth, connective tissue defects, and chronic intra-abdominal pressure; however, the underlying etiologies of POP development are not fully understood, leading to a high burden on patients and the healthcare systems. The uterosacral ligaments are key support structures of the uterus and upper vagina. Our previous work describes observed histopathological changes in uterosacral ligament (USL) tissue and demonstrates the presence of neutrophils in a subgroup of POP individuals. This presence of neutrophils prompted an examination for the presence of a broader spectrum of inflammatory cell types in the USL. Immunohistochemical staining was performed to identify neutrophils, lymphocytes, macrophages, and mast cells outside of the vasculature. All 4 inflammatory cell types were increased in the POP-HQ system-defined POP-Inflammatory (POP-I) phenotype USL tissue relative to the USL tissues of control or other POP-HQ phenotypes. Focal T-lymphocyte and macrophage co-accumulations were observed in the arterial walls from some patients of the POP-vascular (POP-V) phenotype suggesting previous arterial injury. In addition, 1 control and 2 POP-V subjects' USLs contained arterial wall foamy macrophages, evidence of atherosclerosis. These findings further support a complex etiology for POP and indicate that personalized approaches to preventing and treating the condition may be warranted., (© 2024. The Author(s).)
- Published
- 2024
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