The role of E. coli Nissle 1917 in modulating inflammatory cytokine genes in LPS-stimulated THP-1 cells

Inflammation plays a critical role in the pathogenesis of numerous chronic disorders, including cardiovascular diseases, autoimmune conditions, and inflammatory bowel disease (IBD). As a complex immune response, uncontrolled or prolonged inflammation can lead to significant tissue damage and systemic complications. Understanding the molecular mechanisms underlying inflammatory responses is therefore crucial for developing new therapeutic approaches. Escherichia coli Nissle 1917 (EcN), a well-characterized probiotic strain, is known for its immunomodulatory effects on both pro-inflammatory and anti-inflammatory cytokine pathways. This study investigates the impact of EcN supernatant on cytokine expression and secretion profiles in lipopolysaccharide-stimulated (LPS-stimulated) THP-1 cells, an established monocyte-like model for studying inflammation. THP-1 cells were divided into control (unstimulated) and LPS-stimulated groups, with or without EcN supernatant treatment. Gene expression levels of key cytokines, including Interleukin-1β (IL-1β), Tumor Necrosis Factor-α (TNF-α), IL-6, IL-8, and Macrophage Inflammatory Protein-1β (MIP-1β) representing pro-inflammatory cytokines, and IL-10, Transforming Growth Factor beta (TGF-β) representing anti-inflammatory cytokines, were assessed by real-time polymerase chain reaction (real-time PCR). Cytokine secretion levels for TNF-α, IL-1β, and IL-6 were quantified using enzyme-linked immunosorbent assay (ELISA). Results demonstrated that EcN supernatant significantly reduced the LPS-induced upregulation of pro-inflammatory cytokines at both transcriptional and protein levels, while enhancing anti-inflammatory cytokine expression. These findings underscore the potential of EcN-derived supernatants to modulate inflammatory responses, offering insights into their therapeutic role in managing dysregulated immune conditions.