eNOS-derived NO is beneficial in maintaining vascular endothelial integrity, 38 and eNOS-derived NO production suppresses nuclear factor B activity, decreases the transcription of iNOS and intercellular adhesion molecule-1, and prevents lung injury and death due to endotoxin. 39 Thus, NO produced by d7EB cells may protect against iNOS activation and resultant high NO production, which has known deleterious effects on the host. 40 To test this hypothesis, CD11bϩ cells were exposed to an NO donor at a concentration range that induces NO release equivalent to the amount of NO produced by d7EB cells. This experiment reproduced the decreased generation of pro-inflammatory cytokines and reduced the iNOS expression observed in the CD11bϩ cells cocultured with human d7EB cells. Thus, the results suggest a critical role of eNOS-derived NO by d7EB cells in down-regulating iNOS activation in CD11bϩ cells and, thereby, dampening the production of pro-inflammatory cytokines.