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Ann Thorac Surg 2004;77:1222-1227
© 2004 The Society of Thoracic Surgeons
B correlates with enhanced expression of interleukin-1ß and inducible nitric oxide synthase in aged murine lungs to endotoxic stress
a Department of Surgery, Finch University of Health Sciences/The Chicago Medical School at Mount Sinai Hospital Medical Center, Chicago, Illinois, USA
b Department of Surgery, University of South Alabama, Mobile, Alabama, USA
Accepted for publication September 11, 2003.
* Address reprint requests to Dr LoCicero, Department of Surgery, University of South Alabama, 2451 Fillingim St, MSTN 719, Mobile, AL 36617-2293, USA
e-mail: jlocicero{at}usouthal.edu
BACKGROUND: Transcriptional regulation is a major determinant of interleukin-1ß (IL-1ß) protein synthesis. Nuclear factor 
B (NF-B) plays a central role in the regulation of IL-1ß and subsequent IL-1ß-dependent inflammatory processes. Previously, we observed in a murine endotoxic stress model a progressive increase with age in the amount of IL-1ß mRNA. We test the aging pulmonary response of NF-B and NF-B-dependent genes, IL-1ß, 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-1ß production in blood samples and the expression levels of protein and mRNA of IL-1ß and iNOS in lung tissues were measured. NF-B binding activity in lung tissues was also determined.
RESULTS: LPS induced higher levels of IL-1ß in the sera and lungs of senescent mice over young mice. Northern and Western blot analyses showed that mRNA and protein signals of IL-1ß and iNOS were significantly higher in old lungs than in young lungs. Electrophoretic mobility shift assay also showed that NF-B activation was significantly higher in the older animals.
CONCLUSIONS: Our results suggest that elevated activation of NF-B, at least in part, contributes to the dysregulated expression of IL-1ß 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.
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