These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Overexpressed nuclear factor kappaB correlates with enhanced expression of interleukin-1beta and inducible nitric oxide synthase in aged murine lungs to endotoxic stress.
    Author: Chang CK, LoCicero J.
    Journal: Ann Thorac Surg; 2004 Apr; 77(4):1222-7; discussion 1227. PubMed ID: 15063239.
    Abstract:
    BACKGROUND: Transcriptional regulation is a major determinant of interleukin-1beta (IL-1beta) protein synthesis. Nuclear factor kappaB (NF-kappaB) plays a central role in the regulation of IL-1beta and subsequent IL-1beta-dependent inflammatory processes. Previously, we observed in a murine endotoxic stress model a progressive increase with age in the amount of IL-1beta mRNA. We test the aging pulmonary response of NF-kappaB and NF-kappaB-dependent genes, IL-1beta, and inducible nitric oxide synthase (iNOS) in the same model. METHODS: Young (2-month-old) and senescent (25-month-old) mice were given 0.5 mg/kg lipopolysaccharide (LPS) intraperitoneally. Lung and blood samples were harvested after 4 hours. IL-1beta production in blood samples and the expression levels of protein and mRNA of IL-1beta and iNOS in lung tissues were measured. NF-kappaB binding activity in lung tissues was also determined. RESULTS: LPS induced higher levels of IL-1beta in the sera and lungs of senescent mice over young mice. Northern and Western blot analyses showed that mRNA and protein signals of IL-1beta and iNOS were significantly higher in old lungs than in young lungs. Electrophoretic mobility shift assay also showed that NF-kappaB activation was significantly higher in the older animals. CONCLUSIONS: Our results suggest that elevated activation of NF-kappaB, at least in part, contributes to the dysregulated expression of IL-1beta and iNOS in the lungs of senescent animals. Thus increased expression of proinflammatory cytokines and inflammatory responsive genes in the lung may play a role in the increased susceptibility in aging animals to endotoxic stress.
    [Abstract] [Full Text] [Related] [New Search]