CCL2 and cystic fibrosis: Both compounds inhibited the NO production in LPS- and IFN-γ-activated peritoneal macrophages [231]; decreased NF-κB/DNA interactions affecting the IL-8 gene expression in TNF-α treated IB3-1 cells. Inhibited TNF-α induced secretion of monocyte chemoattractant protein-1 (MCP-1) and RANTSE (Regulated on Activation, Normal T cell Expressed and Secreted) as well, suggesting its potential as an anti-inflammatory therapy for cystic fibrosis [336].