ArticleLaboratory investigation; a journal of technical methods and pathology2014
Lactoferrin suppresses the Epstein-Barr virus-induced inflammatory response by interfering with pattern recognition of TLR2 and TLR9.
Article in Laboratory investigation; a journal of technical methods and pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- Androgen Receptor-Induced Lactoferrin Accelerates Prostate Tumorigenesis Through Modulating Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Bovine Lactoferrin Modulates Mononuclear Cell Activity in Human Palatine Tonsils.International journal of molecular sciences · 2026Article
- Tumor-associated characteristics and immune dysregulation in nasopharyngeal carcinoma under the regulation of m7G-related tumor microenvironment cells.World journal of surgical oncology · 2024Article
- The interplay between Epstein-Barr virus DNA and gut microbiota in the development of arthritis in a mouse model.Microbiology spectrum · 2023Article
- The MIF promoter SNP rs755622 is associated with immune activation in glioblastoma.JCI insight · 2023Article
- Time to Kill and Time to Heal: The Multifaceted Role of Lactoferrin and Lactoferricin in Host Defense.Pharmaceutics · 2023Review
- When the allergy alarm bells toll: The role of Toll-like receptors in allergic diseases and treatment.Frontiers in molecular biosciences · 2023Review
- Scratching the Surface Takes a Toll: Immune Recognition of Viral Proteins by Surface Toll-like Receptors.Viruses · 2022Review
- Review
- RNA mImmunity, inflammation and disease · 2021Article
- The potential for Lactoferrin to reduce SARS-CoV-2 induced cytokine storm.International immunopharmacology · 2021Review
- Transcriptional profiling reveals potential involvement of microvillous TRPM5-expressing cells in viral infection of the olfactory epithelium.BMC genomics · 2021Article
- Lactoferrin is a dynamic protein in human melioidosis and is a TLR4-dependent driver of TNF-α release in Burkholderia thailandensis infection in vitro.PLoS neglected tropical diseases · 2020Article
- Clinicopathological and Immunomicroenvironment Characteristics of Epstein-Barr Virus-Associated Gastric Cancer in a Chinese Population.Frontiers in oncology · 2020Article
- Targeting Exosomal EBV-LMP1 Transfer and miR-203 Expression via the NF-κB Pathway: The Therapeutic Role of Aspirin in NPC.Molecular therapy. Nucleic acids · 2019Article
- Early Pattern of Epstein-Barr Virus Infection in Gastric Epithelial Cells by "Cell-in-cell".Virologica Sinica · 2019Article
- Effects and mechanisms of innate immune molecules on inhibiting nasopharyngeal carcinoma.Chinese medical journal · 2019Article
- Epstein-Barr Virus Nuclear Antigen 1 Recruits Cyclophilin A to Facilitate the Replication of Viral DNA Genome.Frontiers in microbiology · 2019Article
- Toll-like receptor-9 in hypoxic nasopharyngeal carcinoma cells and its correlation with cell proliferation and apoptosis.Oncology letters · 2017Article
- Lactoferrin in a Context of Inflammation-Induced Pathology.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epstein-Barr virus (EBV) infection contributes to tumorigenesis of various human malignancies including nasopharyngeal carcinoma (NPC). EBV triggers innate immune and inflammatory responses partly through Toll-like receptor (TLR) signaling. Lactoferrin (LF), with its anti-inflammatory properties, is an important component of the innate immune system. We previously reported that LF protects human B lymphocytes from EBV infection by its ability to bind to the EBV receptor CD21, but whether LF can suppress EBV-induced inflammation is unclear. Here, we report that LF reduced synthesis of IL-8 and monocyte chemoattractant protein-1 (MCP-1) induced by EBV in macrophages via its suppression of NF-κB activity. LF interacted with TLR2 and interfered with EBV-triggered TLR2-NF-κB activation. LF inhibited the ability of TLR9 to recognize dsDNA by binding to its co-receptor CD14, which blocked the interaction between CD14 and TLR9. EBV-induced inflammation was thus aggravated in the presence of CD14. In addition, LF expression levels were significantly downregulated in NPC specimens, and correlated inversely with IL-8 and MCP-1 expression. These findings suggest that LF may suppress the EBV-induced inflammatory response through interfering with the activation of TLR2 and TLR9.
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