IL-8/CXCL8 is a CXC chemokine produced during inflammation that activates neutrophils, inducing chemotaxis, exocytosis, respiratory burst, and neutrophil accumulation in vivo
[1]. Mechanistically, IL-8 acts through CXCR1/CXCR2 to control target-cell adhesion, migration, and function, while downstream signaling supports actin remodeling, calcium mobilization, granule exocytosis, and respiratory burst
[2]. In inflammatory and cancer contexts, the CXCL8-CXCR1/2 axis participates in inflammatory mediator trafficking, tumor progression, metastasis, and diseases including COPD, asthma, cystic fibrosis, and cancer
[3]. Compared with related ELR
+ CXC chemokines, IL-8 is distinguished by dual activation of CXCR1 and CXCR2, whereas CXCR2 also recognizes CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, and CXCL7
[4]. CXCL8 monomers and dimers differentially regulate CXCR1 and CXCR2, supporting receptor-selective experimental designs for neutrophil recruitment and cytotoxic activity studies
[4]. For experimental applications, noncompetitive allosteric CXCR1/CXCR2 inhibitors block inflammatory CXCL8 receptor signaling, and CXCL8-derived antagonists can reduce neutrophil infiltration in inflammatory models
[5][6].