作者: Jack B. Cowland , Tatsushi Muta , Niels Borregaard
DOI: 10.4049/JIMMUNOL.176.9.5559
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摘要: Neutrophil gelatinase-associated lipocalin (NGAL) is a siderophore-binding protein that exerts bacteriostatic effect by sequestering iron. Strong induction of NGAL synthesis has been observed in inflamed epithelium the lungs and colon. Expression up-regulated lung epithelial cell line A549 IL-1beta, but not TNF-alpha, despite an NF-kappaB binding to promoter both cytokines. In this study, we present evidence IL-1beta specificity caused requirement for NF-kappaB-binding cofactor IkappaB-zeta transcriptional activation. Up-regulation expression cells following stimulation was dependent on de novo greatly diminished small interfering against mRNA. Cotransfection with plasmid expressing made TNF-alpha capable inducing transcription, indicating only factor discriminating between their ability induce expression. Coexpression Bcl-3, which closely related IkappaB-zeta, did enable transcription. A functional site required exert its effect. The human beta defensin 2 gene also IL-1beta-specific cells. Our findings indicate common regulatory mechanism evolved control subset antimicrobial proteins expressed