Linked Life Data

18256171

Source:http://linkedlifedata.com/resource/pubmed/id/18256171

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-4-18
pubmed:abstractText
Cigarette smoking is associated with the development of inflammatory lung diseases representing major health problems world-wide. We hypothesized that the redox-regulating molecule thioredoxin-1 (TRX), which shows anti-inflammatory, antioxidative, and antiapoptotic effects, could be induced by cigarette smoke (CS) and contribute to protect against CS-induced inflammation and lung destruction. In an acute study, human TRX transgenic mice and C57BL6/J mice were exposed to mainstream CS for 3 days. In the lungs of CS-exposed mice, bronchial epithelial injury and bronchoalveolar lavage neutrophilia were observed. Oxidative stress and apoptosis were enhanced, and the expression of cytokines macrophage inflammatory protein-2 and tumor necrosis factor (TNF)-alpha was increased 15.3- and 2.4-fold, respectively. Compared with C57BL6/J mice, TRX-transgenic mice had significantly less inflammation, oxidative damage, and apoptosis, as well as decreased levels of matrix metalloprotease-12 mRNA and serum TNF-alpha. When recombinant human TRX (40 microg/body/day, 3 days) was injected i.p. into CS-exposed C57BL6/J mice, a significant effect to offer protection against CS-induced lung injury was observed through suppression of neutrophil influx. In the chronic study, TRX-transgenic mice and C57BL6/J mice were exposed to CS for 6 months. This chronic exposure caused pulmonary emphysema in C57BL6/J mice accompanying prominent infiltration of macrophages and neutrophils to lung. These pathological changes were significantly suppressed in TRX-transgenic mice. In conclusion, TRX induction ameliorated CS-induced lung inflammation and emphysema in mice. TRX-1 may therefore play a preventive or therapeutic role in lung inflammatory disorders such as chronic obstructive pulmonary disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1521-0103
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
325
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
380-8
pubmed:meshHeading
pubmed-meshheading:18256171-Animals, pubmed-meshheading:18256171-Anti-Inflammatory Agents, pubmed-meshheading:18256171-Apoptosis, pubmed-meshheading:18256171-Bronchoalveolar Lavage Fluid, pubmed-meshheading:18256171-Chemokine CXCL2, pubmed-meshheading:18256171-Humans, pubmed-meshheading:18256171-Macrophages, pubmed-meshheading:18256171-Male, pubmed-meshheading:18256171-Matrix Metalloproteinase 12, pubmed-meshheading:18256171-Mice, pubmed-meshheading:18256171-Mice, Inbred C57BL, pubmed-meshheading:18256171-Mice, Transgenic, pubmed-meshheading:18256171-Neutrophils, pubmed-meshheading:18256171-Oxidative Stress, pubmed-meshheading:18256171-Pneumonia, pubmed-meshheading:18256171-Pulmonary Emphysema, pubmed-meshheading:18256171-RNA, Messenger, pubmed-meshheading:18256171-Recombinant Proteins, pubmed-meshheading:18256171-Smoke, pubmed-meshheading:18256171-Thioredoxins, pubmed-meshheading:18256171-Tobacco, pubmed-meshheading:18256171-Tumor Necrosis Factor-alpha
pubmed:year
2008
pubmed:articleTitle
Thioredoxin-1 ameliorates cigarette smoke-induced lung inflammation and emphysema in mice.
pubmed:affiliation
Department of Experimental Therapeutics, Translational Research Center, Kyoto University Hospital, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto, 6068507 Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't