Effect of NF-κB Deletion on Bone Marrow Macrophage Respiratory Burst Ability

Abstract

The nuclear factor-kappaB (NF-κB) signaling pathway is very important in normal immune system function and is also often aberrantly regulated in many different types of cancers. As many cancers are characterized by elevated numbers of infiltrating monocytes/macrophages, we have developed an animal model that lacks canonical NF-κB signaling in bone-marrow derived macrophages (BMDMs). As BMDMs can infiltrate solid cancers, the aim of this particular study was to assess the functionality of phagocyte oxidase ability in NF-κB deficient BMDMs. A respiratory burst assay involves stimulating the phagocyte oxidase enzyme in macrophages to release reactive oxygen species (ROS) so that they can degrade and combat invading pathogens as well as cancer cells. Based on our recent experiments that showed BMDMs lacking p65 had poor phagocytosis ability and low nitrite production, we hypothesize that BMDMs lacking NF-κB signaling will have a decreased respiratory burst response compared to control BMDMs.