# Exploring the effects of IFN-τ on LPS-induced endometritis in cows based on transcriptomics

**Authors:** Pan Liu, Yaofeng Zhang, Xu Chen, Lijun Tang, Wenxiu Xu, Guigui Wang, Duoqi Zhang, Junfeng Liu, Vikash Chandra, Vikash Chandra, Vikash Chandra

PMC · DOI: 10.1371/journal.pone.0343553 · 2026-03-05

## TL;DR

This study explores how IFN-τ affects LPS-induced inflammation in cow endometrial cells using transcriptomics to identify key pathways and potential therapeutic targets.

## Contribution

The study reveals novel regulatory networks of IFN-τ in modulating inflammation via multiple synergistic pathways in bovine endometritis.

## Key findings

- IFN-τ modulates LPS-induced inflammation in bovine endometrial cells through multiple synergistic pathways.
- Transcriptomic analysis identified 109, 1109, and 962 differentially expressed mRNAs across treatment groups.
- Key pathways include NF-κB, cytokine signaling, and antigen processing, highlighting IFN-τ's anti-inflammatory role.

## Abstract

Endometritis in dairy cows is a common reproductive disease that severely affects reproductive performance and milk production, resulting in significant economic losses. Lipopolysaccharide (LPS) as a PAMP capable of inducing inflammatory responses in the endometrium through the NF-κB pathway. Interferon-tau (IFN-τ) is a type I interferon with significant anti-inflammatory properties. Currently, transcriptomics sequencing technology has gradually become an attractive tool for studying such diseases. This study established an inflammatory model of bovine endometrial cells (BENDs) using LPS induction and employed RNA-seq technology to investigate the expression profiles of mRNAs in BENDs from the Control group (C), the LPS-treated group (L), and the IFN-τ + LPS-treated group (F). The results showed that there were 109, 1109, and 962 Differentially Expressed mRNAs (DEmRNAs) in the C vs L, C vs F, and L vs F. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis showed that these DEmRNAs were mainly involved in the regulation of host immune responses (e.g., NOD-like receptor signaling pathway, IL-17 signaling pathway and RIG-I-like receptor signaling pathway, NF-kappa B signaling pathway), signal transduction molecules and interactions (e.g., Cytokine-cytokine receptor interaction; Cell adhesion molecules), metabolic process (e.g., Glycosphingolipid biosynthesis-lacto and neolacto series) and Antigen processing and presentation, Complement and coagulation cascades, Th17 cell differentiation, etc. biological process. This study not only elucidates the molecular mechanisms by which BENDs respond to microbial invasion but also reveals the specific regulatory network through which IFN-τ exerts its anti-inflammatory effects via multiple synergistic pathways. It provides crucial theoretical support for the clinical application of interferon therapy in treating endometritis, demonstrating significant research value and promising applications.

## Linked entities

- **Proteins:** IFNT (interferon-tau 3g), IRF6 (interferon regulatory factor 6), NFKB1 (nuclear factor kappa B subunit 1)
- **Diseases:** endometritis (MONDO:0000918)
- **Species:** Bos taurus (taxon 9913)

## Full-text entities

- **Genes:** CD38 (CD38 molecule) [NCBI Gene 327677], CD79A (CD79a molecule) [NCBI Gene 973] {aka IGA, IGAlpha, MB-1, MB1}, IL17A (interleukin 17A) [NCBI Gene 282863] {aka IL-17, IL17}, IFNAR2 (interferon alpha and beta receptor subunit 2) [NCBI Gene 282258] {aka IFN-R, IFN-R-2, IFNBR}, OXTR (oxytocin receptor) [NCBI Gene 281371], IFNG (interferon gamma) [NCBI Gene 281237], PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) [NCBI Gene 282306], AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 280991] {aka AKT}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, CD4 (CD4 molecule) [NCBI Gene 407098], TLR4 (toll like receptor 4) [NCBI Gene 281536], IL10 (interleukin 10) [NCBI Gene 281246] {aka IF2A}, IFNT2 (interferon tau) [NCBI Gene 317698] {aka IFN-tau-c2, IFNT, IFNT1, TP-1}, TNF (tumor necrosis factor) [NCBI Gene 280943] {aka TNF-a, TNF-alpha, TNFa}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 280828] {aka IL-8, IL8}, IL1B (interleukin 1 beta) [NCBI Gene 281251], LOC517016 (interleukin 6 (interferon, beta 2)) [NCBI Gene 517016] {aka IF1DA6}, IFNA16 (interferon, alpha 16) [NCBI Gene 510726] {aka IFN}, IFN-TAU (interferon-tau-like) [NCBI Gene 509166] {aka IF1BE10}, ESR1 (estrogen receptor 1) [NCBI Gene 407238], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, HADHA (hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit alpha) [NCBI Gene 281810], IL4 (interleukin 4) [NCBI Gene 280824] {aka BSF-1, IL-4}
- **Diseases:** infection (MESH:D007239), tumors (MESH:D009369), BENDs (MESH:D002418), inflammation (MESH:D007249), pain (MESH:D010146), Endometritis (MESH:D004716), reproductive disease (MESH:D060737), hearing loss (MESH:D034381), infectious diseases (MESH:D003141)
- **Chemicals:** lactose (MESH:D007785), nitrogen (MESH:D009584), GSL (MESH:D006028), fatty acid (MESH:D005227), streptomycin (MESH:D013307), GTP (MESH:D006160), cADPR (MESH:D036563), DMEM-H (-), NAADP (MESH:C024376), penicillin (MESH:D010406), sphingolipid (MESH:D013107), PBS (MESH:D007854), NAD (MESH:D009243), Progesterone (MESH:D011374), PGF2 (MESH:D015237), PolyA (MESH:D011061), calcium (MESH:D002118), CO2 (MESH:D002245), lipid (MESH:D008055), LPS (MESH:D008070), agarose (MESH:D012685), Apigenin (MESH:D047310)
- **Species:** Escherichia coli (E. coli, species) [taxon 562], Human immunodeficiency virus 1 (no rank) [taxon 11676], Ovis aries (domestic sheep, species) [taxon 9940], Bos taurus (bovine, species) [taxon 9913]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12962510/full.md

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Source: https://tomesphere.com/paper/PMC12962510