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Induced Uterine Infection Perturbs Bovine Endometrial Function

ABSTRACT: Uterine diseases in dairy cattle are associated with reduced fertility, but the specific mechanisms of disease mediated subfertility are not fully elucidated. We hypothesized that an intrauterine infusion of Escherichia coli and Trueperella pyogenes would alter the endometrial transcriptome at a time coincident with conceptus elongation, and compromise oocyte developmental competence. Sixty-one non-lactating Holstein cows received an intrauterine infusion of either saline (n = 29) or pathogenic E. coli and T. pyogenes (n = 32) to induce acute endometrial inflammation. Endometrial samples were collected via cytobrush 41 d after infusion and analyzed by RNA sequencing. Bacteria infusion altered the expression of 203 genes in the endometrium 41 d after infusion. Top upregulated genes were GSTA3, PVALB, JAKMIP2, FOLH1B, TCF23, and top downregulated genes were MYMK, LOC104974498, CDRT1, KIAA0408, SLC45A2. The differentially expressed genes were functionally annotated to 54 canonical pathways with glutathione-mediated detoxification being the top predicted pathway altered following bacteria infusion. Collectively, this work demonstrates that bacterial infections can have lasting effects on the uterus which may provide a link to the long-term subfertility of cows after uterine disease.

ORGANISM(S): Bos taurus

PROVIDER: GSE292954 | GEO | 2026/01/26

REPOSITORIES: GEO

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Project description:Background: Physiological inflammation of the uterus postpartum is essential for the reparative processes of involution after calving. In the majority of cows, this inflammation is resolved and homeostasis is restored. However, in a significant subset, inflammation persists and contributes to tissue damage, pathology and subfertility. Transcriptomic differences of immune genes between cattle that resolve inflammation and those that develop uterine disease have been detected as early as 7 days postpartum (DPP) suggesting that the host immune response plays an important role in disease outcome. Results: Here, we extensively characterise the immune response at the transcriptomic level in endometrial epithelial cells from post-partum dairy cows phenotyped for both clinical and sub-clinical forms of uterine disease. We address the hypothesis that excessive expression of endometrial inflammatory molecules contributes to development of endometritis. Classification of cattle (n=112) as healthy or with uterine disease (purulent vaginal discharge; PVD and cytological endometritis; CYTO) was based on vaginal mucus score and >18% polymorphonuclear cell infiltrate into the endometrium at 21 DPP. RNA-seq analysis of endometrial epithelial cells collected using cytobrushes identified differential expression of 294 genes (FDR <0.05) between cows that subsequently resolved inflammation (n=10) and those that developed disease (n=20). Pathway over-representation analysis of differentially expressed genes (DEG) identified significant changes in immune-related pathways, including the NOD-like receptor signalling pathway, cytokine-cytokine receptor interaction pathway and the Toll-like receptor signalling pathway which were up-regulated in cattle that subsequently developed disease. The majority of the DEG were upregulated in cows that developed PVD, and included all genes upregulated in CYTO cows, suggesting a core inflammatory gene signature early post-partum contributes to the onset of uterine disease. This inflammatory signature was validated by qPCR in an independent group of cows (n=56) and included upregulation of pro-inflammatory genes (including TLR2, TLR4, NLRP3, IL1A, IL1B, IL8, and S100A8) at day 7 postpartum in cows that failed to resolve inflammation. Conclusions: Despite a large amount of inter-animal heterogeneity, these results suggest that excessive activation and inappropriate regulation of the inflammatory response early postpartum is a key feature of the subsequent development of uterine disease. Keywords: Endometritis, Inflammation, Transcriptome, Next generation sequencing, Dairy cattle, Uterine involution, Immune response

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Induced Uterine Infection Perturbs Bovine Endometrial Function

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