Abstract
Introduction: Toll receptors are vital to the innate immune system. They recognize common microbial pathogen molecular patterns. The signaling pathways activated produce proinflammatory cytokines and type I interferons to start the immune response to infection. Inflammatory, autoimmune, and cancer diseases are connected to signaling abnormalities. Thus, toll receptor expression patterns and control mechanisms are essential for immune response research and treatment.
Methods: Metadichol, a nanoemulsion of long-chain alcohol, was applied to peripheral blood mononuclear cells to evaluate the expression of all ten toll receptor family members (TLR1-10), MYD88, and downstream genes (IRAK4, TRAF3, TRAF6 and TRIF). Quantitative real-time PCR measured gene expression.
Results: Toll receptors 1–10 responded as inverted U-shaped to Metadichol treatment, except Toll receptor 4. Metadichol affects TLR expression differently at low, moderate, and high dosages. Metadichol activated all 15 genes, including TLRs and downstream signalizing molecules.
Importing 15 genes into Pathway Studio produced a gene expression network analysis. Gene set enrichment analysis (GSEA) used the proprietary Elsevier pathway collection. An enriched gene list with more gene interactions than expected for a random gene collection of similar size and distribution indicated a significant biological relationship between these genes.
Conclusions: Metadichol expresses all the toll receptors, the MYD88 gene, and four other downfield genes. Since all immune cells express TLRs, this leads to a more robust solution for activating innate and adaptive immunity processes in humans.