Linked Life Data

14680365

Source:http://linkedlifedata.com/resource/pubmed/id/14680365

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2003-12-18
pubmed:abstractText
We have previously demonstrated in alveolar macrophages that aging is associated with a decline in lipopolysaccharide-induced tumor necrosis factor-alpha production. The purpose of the present study was to investigate the immunotoxicological consequences of this defective activation in an experimental model of acute silicosis. Young (3 months old) and old (>18 months old) rats were intratracheally instilled with silica or saline as control. In young animals, as expected, silica induced a significant increase in bronchoalveolar lavage fluid of tumor necrosis factor-alpha, lactate dehydrogenase, and cell numbers, which correlated with increased collagen deposition and silicotic nodule formations. On the contrary, in old rats, no changes in bronchoalveolar lavage fluid or lung parameters were observed, indicating that senescent rats are resistant to the acute effects of silica. These in vivo results were confirmed in vitro, where silica-induced tumor necrosis factor-alpha release was drastically reduced in alveolar macrophages obtained from old animals. This could be explained with a defective protein kinase C betaII translocation in aged macrophages, due to decreased expression of its anchoring protein RACK-1. Furthermore, a decrease in FAS-L expression and silica-induced apoptosis in old macrophages was observed, supporting the idea that age-associated alterations in signal transduction pathways contribute to decreased sensitivity to silica-induced acute lung fibrosis in old animals.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0893-228X
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1520-7
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:14680365-Acute Disease, pubmed-meshheading:14680365-Aging, pubmed-meshheading:14680365-Animals, pubmed-meshheading:14680365-Apoptosis, pubmed-meshheading:14680365-Bronchoalveolar Lavage Fluid, pubmed-meshheading:14680365-Cell Membrane, pubmed-meshheading:14680365-Cytosol, pubmed-meshheading:14680365-Disease Models, Animal, pubmed-meshheading:14680365-Fas Ligand Protein, pubmed-meshheading:14680365-L-Lactate Dehydrogenase, pubmed-meshheading:14680365-Lung, pubmed-meshheading:14680365-Macrophages, Alveolar, pubmed-meshheading:14680365-Male, pubmed-meshheading:14680365-Membrane Glycoproteins, pubmed-meshheading:14680365-Protein Kinase C, pubmed-meshheading:14680365-Rats, pubmed-meshheading:14680365-Rats, Sprague-Dawley, pubmed-meshheading:14680365-Receptors, Cell Surface, pubmed-meshheading:14680365-Silicon Dioxide, pubmed-meshheading:14680365-Silicosis, pubmed-meshheading:14680365-Tumor Necrosis Factor-alpha
pubmed:year
2003
pubmed:articleTitle
Resistance to acute silicosis in senescent rats: role of alveolar macrophages.
pubmed:affiliation
Laboratory of Toxicology, Department of Pharmacological Sciences, University of Milan, Via Balzaretti 9, 20133 Milan, Italy. emanuela.corsini@unimi.it
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't