Induction of neutrophil gelatinase-associated lipocalin expression by co-stimulation with interleukin-17 and tumor necrosis factor-alpha is controlled by IkappaB-zeta but neither by C/EBP-beta nor C/EBP-delta.

Neutrophil gelatinase-associated lipocalin (NGAL) is a siderophore-binding antimicrobial protein that is up-regulated in epithelial tissues during inflammation. We demonstrated previously that the gene encoding NGAL (LCN2) is strongly up-regulated by interleukin (IL)-1beta in an NF-kappaB-dependent manner but not by tumor necrosis factor (TNF)-alpha, another potent activator of NF-kappaB. This is due to an IL-1beta-specific synthesis of the NF-kappaB-binding co-factor IkappaB-zeta, which is essential for NGAL induction.

No detectable Chlamydia pneumoniae and cytomegalovirus DNA in leukocytes in subjects with echolucent and echogenic carotid artery plaques.

Background: Controversy exists whether persistent Chlamydia pneumoniae or cytomegalovirus infections cause initiation or progression of atherosclerosis. C. pneumoniae DNA in peripheral blood mononuclear cells (PBMC) has been proposed to be a more reliable marker of cardiovascular risk than are C.