Multimodal Profiling of Repair-Associated Immune Dynamics in a Mouse Model of Menstruation

Rebecca J. Ainslie, Ainslie RJ, Kirkwood PM, Li H, Gerasimou S, Philippa T. K. Saunders, Simitsidellis I, Douglas A Gibson
2026 · doi:10.64898/2026.02.06.704418
preprint OA: gold CC-BY-4.0
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⚙ AI-generated summary by qwen3.7-flash, 2026-08-20 ⓘ

Single-cell and spatial analyses of a mouse menstruation model reveal that monocytes, macrophages, and neutrophils drive endometrial repair via thrombospondin 1 and secreted phosphoprotein 1 signaling pathways.

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Researchers utilized single-cell RNA sequencing and multiplex immunohistochemistry to characterize uterine immune cells in a mouse model of simulated menstruation. The study identified distinct compositional changes across tissue breakdown, repair, and remodeling phases, highlighting predominant roles for monocytes, macrophages, and neutrophils in endometrial repair. Key signaling pathways involving thrombospondin 1 and secreted phosphoprotein 1 were implicated in this process through bioinformatic analysis. Relevance to endometriosis: the paper provides fundamental insights into menstrual physiology and endometrial repair mechanisms that are directly relevant to understanding the pathophysiology of endometriosis.

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Abstract

Despite the importance of inflammation to menstruation, we lack detailed understanding of how immune dynamics contribute to endometrial repair. We performed detailed phenotypic characterisation of uterine immune cells using single cell RNA sequencing, flow cytometry and multiplex immunohistochemistry in a mouse model of simulated menstruation. Uterine tissues were collected from age-matched controls or from key phases of menstruation, including tissue breakdown, repair and remodelling. Our findings reveal distinct compositional changes across different phases of menstruation and highlight predominant roles for monocytes, macrophages, and neutrophils in endometrial repair. Immunohistochemistry revealed the spatial association of these myeloid cell subsets with areas of tissue repair and remodelling. Bioinformatic analysis highlighted key roles for monocyte, macrophage and neutrophil signalling during endometrial repair with thrombospondin 1 and secreted phosphoprotein 1 emerging as key signalling pathways. These data significantly advance our understanding of menstrual physiology and identify potential therapeutic targets for menstrual disorders. summary This study investigates immune cell dynamics in a mouse model of menstruation, highlighting roles for monocytes, macrophages, and neutrophils in non-fibrotic endometrial repair, and identifies key signalling pathways as potential therapeutic targets for menstrual disorders.
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Abstract Despite the importance of inflammation to menstruation, we lack detailed understanding of how immune dynamics contribute to endometrial repair. We performed detailed phenotypic characterisation of uterine immune cells using single cell RNA sequencing, flow cytometry and multiplex immunohistochemistry in a mouse model of simulated menstruation. Uterine tissues were collected from age-matched controls or from key phases of menstruation, including tissue breakdown, repair and remodelling. Our findings reveal distinct compositional changes across different phases of menstruation and highlight predominant roles for monocytes, macrophages, and neutrophils in endometrial repair. Immunohistochemistry revealed the spatial association of these myeloid cell subsets with areas of tissue repair and remodelling. Bioinformatic analysis highlighted key roles for monocyte, macrophage and neutrophil signalling during endometrial repair with thrombospondin 1 and secreted phosphoprotein 1 emerging as key signalling pathways. These data significantly advance our understanding of menstrual physiology and identify potential therapeutic targets for menstrual disorders. summary This study investigates immune cell dynamics in a mouse model of menstruation, highlighting roles for monocytes, macrophages, and neutrophils in non-fibrotic endometrial repair, and identifies key signalling pathways as potential therapeutic targets for menstrual disorders. Competing Interest Statement The authors have declared no competing interest. Footnotes Figure files updated to higher resolution to improve readability of gene names in scRNAseq data

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