Abstract
Under inflammatory situations, endoplasmic reticulum (ER) stress occurs at local sites and modulates inflammatory processes. NF-κB is a key regulator for immune and inflammatory responses, and its activity is influenced by ER stress positively or negatively. Recent investigation suggested that ER stress induces activation of NF-κB in the early phase, whereas in the later phase, consequent unfolded protein response (UPR) inhibits NF-κB. This review summarizes current knowledge on potential mechanisms underlying the biphasic, bidirectional regulation of NF-κB by the UPR and possible roles for ER stress in the regulation of inflammation.