Tumor necrosis factor-alpha-induced interleukin-8 production (TNF-α-induced IL-8 production)

Tumor necrosis factor-alpha (TNF-α)-induced interleukin-8 (IL-8) production is a pro-inflammatory signaling process rather than a single molecular target. This cascade begins when the cytokine TNF-α binds to its cognate receptors, primarily TNF receptor 1 (TNFR1), on the surface of various cell types such as macrophages and endothelial cells (Source: UniProt P01375, P19438). This binding event triggers intracellular signaling pathways, most notably the NF-κB and MAPK pathways, which culminate in the transcriptional activation and secretion of IL-8 (Source: PubMed PMID: 12631597). IL-8, also known as CXCL8, serves as a potent chemoattractant for neutrophils, playing a critical role in the recruitment of immune cells to sites of inflammation (Source: UniProt P10145). In drug discovery, measuring the inhibition of TNF-α-induced IL-8 production is a standard functional assay used to screen for anti-inflammatory compounds and biologics. Therapeutic agents like infliximab and adalimumab target this process by neutralizing TNF-α, thereby preventing the downstream production of IL-8 and reducing tissue inflammation (Source: StatPearls, TNF Inhibitors). Dysregulation of this pathway is central to the pathogenesis of chronic inflammatory diseases, including rheumatoid arthritis, Crohn's disease, and plaque psoriasis. Because it represents a multi-step biological response involving several proteins, it is classified as a signaling event or assay endpoint rather than a discrete therapeutic target.

Other names

TNF-alpha-induced CXCL8 productionTNF-stimulated IL-8 releaseTNF-alpha/IL-8 axisTNF-alpha-induced chemokine secretion

Neutralization of soluble and transmembrane TNF-alpha or inhibition of its receptors to block the signaling cascade that leads to IL-8 gene expression and secretion.