ArticleOdontology2026
Enterococcus faecalis and lipoteichoic acid up-regulated PD-L1 of macrophage through TLR and IRE1 α/XBP1 signaling axis.
Article in Odontology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Highly Alkaline-ResistantMicroorganisms · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
Programmed death-ligand 1 (PD-L1) is a critical immune checkpoint molecule that negatively regulates T-cell activation and serves as a characteristic marker of exhausted T cells in bacterial and viral infections. In this study, we found that Enterococcus faecalis (E. faecalis) infection modulated macrophage immune function under inflammatory conditions by upregulating PD-L1 expression. The aim of this study was to investigate the effect and potential regulatory mechanisms of E. faecalis and its virulence factor lipoteichoic acid (LTA) on the expression of PD-L1 in macrophages. RAW264.7 cells were treated with E. faecalis or LTA, respectively. Cellular immunofluorescence staining, flow cytometry, quantitative real time polymerase chain reaction (qRT-PCR) and Western blotting (WB) were employed to assess the expression of PD-L1 and endoplasmic reticulum (ER) stress-related proteins, including inositol-requiring enzyme 1 α (IRE1 α) and X-box binding protein 1 (XBP1), in macrophages. Following inhibition of the IRE1 α/XBP1 pathway and treatment with E. faecalis, qRT-PCR, flow cytometry, and WB were performed to detect the expression of PD-L1 and XBP1. Macrophage apoptosis was quantified by flow cytometry. Toll-like receptor 2 (TLR2) was knocked down using small interfering RNA (siRNA), and the expression of PD-L1, IRE1 α, and XBP1 in TLR2-silenced macrophages stimulated by E. faecalis was evaluated by qRT-PCR and WB. Statistical significance was analyzed using the Mann-Whitney test and Kruskal-Wallis test. The results demonstrated that E. faecalis and LTA significantly enhanced the expression of PD-L1, IRE1 α, and XBP1s in macrophages. Inhibition of the IRE1 α/XBP1 pathway reduced XBP1s and PD-L1 expression as well as apoptosis in E. faecalis-stimulated macrophages. TLR2 silencing decreased PD-L1, IRE1 α, and XBP1s expression levels in E. faecalis-stimulated macrophages. These findings reveal a novel mechanism by which E. faecalis induces persistent apical periodontitis and provide a foundation for further exploration of immune checkpoint molecules in the pathogenesis and treatment of this disease.
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Registered trials
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