Inflammation and hepatocyte damage augment Hepcidin transcription and iron sequestration via several pathways. LPS released by bacterial infection activates TLR-4 signaling, which increases IL-6 release by macrophages. IL-6 signaling leads to phosphorylation of Stat3 and increased Stat3 binding to the Hepcidin promoter, whereas endoplasmic reticulum (ER) stress in hepatocytes promotes CEBP-α binding to the Hepcidin promoter. BMP signaling via ligands, such as BMP2, BMP4, BMP6, and BMP9 activating BMP receptor-I, causes Smad phosphorylation and Smad binding to the Hepcidin promoter, which is required for Hepcidin transcription. The BMP coreceptor hemojuvelin (HJV) interacts with the BMP receptor to enhance BMP signaling. Inflammation also promotes macrophage release of lipocalin, which can interact with bacterial siderophores to sequester iron.