Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1997-10-17
pubmed:abstractText
Fas antigen is a cell surface protein that mediates apoptosis, and it is expressed in various cells and tissues. Fas ligand binds to its receptor Fas, thus inducing apoptosis of Fas-bearing cells. Malfunction of the Fas-Fas ligand system causes lymphoproliferative disorders and autoimmune diseases, whereas its exacerbation may cause tissue destruction. We hypothesize that excessive apoptosis mediated by Fas-Fas ligand interaction may damage alveolar epithelial cells and result in pulmonary fibrosis. Mice were allowed to inhale repeatedly an aerosolized anti-Fas antibody for 14 days. The nuclei of bronchial and alveolar epithelial cells were positively stained by in situ DNA nick end labeling. Electron microscopy demonstrated apoptotic changes in bronchial and alveolar epithelial cells. Histologic findings and hydroxyproline content showed the development of pulmonary fibrosis, which was dependent on the dose of anti-Fas antibody. The repeated inhalation of control antibody (isotype-matched control hamster IgG) did not induce apoptosis of epithelial cells or pulmonary fibrosis. The expression of TGF-beta mRNA was upregulated from day 7 to day 28 in lung tissues of anti-Fas antibody-treated mice but not in those of control mice. In this report, we present the evidence that repeated inhalation of anti-Fas antibody mimicking Fas-Fas ligand crosslinking induces excessive apoptosis and inflammation, which results in pulmonary fibrosis in mice.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1044-1549
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
272-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9308912-Animals, pubmed-meshheading:9308912-Antibodies, pubmed-meshheading:9308912-Antigens, CD95, pubmed-meshheading:9308912-Apoptosis, pubmed-meshheading:9308912-Biotin, pubmed-meshheading:9308912-Bronchoalveolar Lavage Fluid, pubmed-meshheading:9308912-Cross-Linking Reagents, pubmed-meshheading:9308912-DNA Fragmentation, pubmed-meshheading:9308912-Deoxyuracil Nucleotides, pubmed-meshheading:9308912-Epithelial Cells, pubmed-meshheading:9308912-Epithelium, pubmed-meshheading:9308912-Gene Expression, pubmed-meshheading:9308912-Hydroxyproline, pubmed-meshheading:9308912-Ligands, pubmed-meshheading:9308912-Lymphotoxin-alpha, pubmed-meshheading:9308912-Mice, pubmed-meshheading:9308912-Mice, Inbred ICR, pubmed-meshheading:9308912-Microscopy, Electron, pubmed-meshheading:9308912-Pulmonary Alveoli, pubmed-meshheading:9308912-Pulmonary Fibrosis, pubmed-meshheading:9308912-Staining and Labeling, pubmed-meshheading:9308912-Tumor Necrosis Factor-alpha
pubmed:year
1997
pubmed:articleTitle
Induction of apoptosis and pulmonary fibrosis in mice in response to ligation of Fas antigen.
pubmed:affiliation
Faculty of Medicine, Research Institute for Diseases of the Chest, Kyushu University, Higashiku, Fukuoka, Japan. hagimoto@j-pal.or.jp
pubmed:publicationType
Journal Article