NF-κB-mediated inverse regulation of fractalkine and CX3CR1 during CLP-induced sepsis

► Downregulation of CX3CR1 receptor expression during CLP-induced sepsis. ► Upregulation of the expression of the ligand CX3C chemokine fractalkine in septic mice. ► This inverse regulation during sepsis is likely mediated by proinflammatory cytokines. ► NF-κB plays a superior role in the regulation of fractalkine and CX3CR1 receptor. ► Blocking of NF-κB results in a amelioration of septic regulation of fractalkine and CX3CR1 receptors.