Linked Life Data

20490462

Source:http://linkedlifedata.com/resource/pubmed/id/20490462

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2010-11-25
pubmed:abstractText
Pulmonary silicosis is a deadly disease which kills thousands of people every year worldwide. The disease initially develops as an inflammatory response with recruitment of inflammatory cells into the lung controlled by multiple cytokines. The question whether these cytokines exert biological functions through signal transducing pathway remains unanswered along with the potential role of interleukin-6 receptor ? (IL-6R?) in regulating inflammatory cytokines. We aimed to assess the status of signal transducers and activator of transcription (Stat3), suppressor of cytokine signalling 3(Socs3) and inflammatory cytokines in airways of silica-exposed mice, and their relationship with IL-6R?. Silica-exposed and silica-exposed IL-6R? gene knockdown Balb/c mice were used in the study. Lung function was measured by plethysmography, mRNA expression of cytokines and signal molecules by qRT(2)-PCR and lung architecture by histopathology; T helper cell-type 2 (Th2) cytokines in broncho-alveolar lavage fluids were evaluated by ELISA and hydroxyproline in lung by colorimetry. Elevated levels of collagen deposition, signs of lung fibrosis, infiltration of inflammatory cells and presence of exfoliated mucosa in the lung of silica-exposed mice with concurrent increase in methacholine-induced specific resistance of airways were observed on day 60 post-exposure. In parallel, heightened expression of Th2 cytokines (IL-4, IL-5, IL-6) and signal molecules (Stat3 and Socs3) were observed in the airways of silica-exposed mice. Th1 (IL-1? and TNF-?) cytokines are underexpressed in majority of the airways tissues of silica-exposed mice. Silencing IL-6R? in lung of silica-exposed mice down regulated the hypermorphic mRNA pool of potential Th2 cytokines and signal molecules. Hypermorphic expression of Th2 cytokines and signal molecules in airways of silica-exposed mice are mediated through IL-6R?.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1432-0738
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
947-55
pubmed:meshHeading
pubmed-meshheading:20490462-Animals, pubmed-meshheading:20490462-Bronchoalveolar Lavage Fluid, pubmed-meshheading:20490462-Colorimetry, pubmed-meshheading:20490462-Cytokines, pubmed-meshheading:20490462-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:20490462-Female, pubmed-meshheading:20490462-Hydroxyproline, pubmed-meshheading:20490462-Inflammation, pubmed-meshheading:20490462-Interleukin-6, pubmed-meshheading:20490462-Lung, pubmed-meshheading:20490462-Mice, pubmed-meshheading:20490462-Mice, Inbred BALB C, pubmed-meshheading:20490462-Pulmonary Fibrosis, pubmed-meshheading:20490462-RNA, Messenger, pubmed-meshheading:20490462-Receptors, Interleukin-6, pubmed-meshheading:20490462-STAT3 Transcription Factor, pubmed-meshheading:20490462-Silicon Dioxide, pubmed-meshheading:20490462-Silicosis, pubmed-meshheading:20490462-Suppressor of Cytokine Signaling Proteins, pubmed-meshheading:20490462-Th2 Cells, pubmed-meshheading:20490462-Tumor Necrosis Factor-alpha
pubmed:year
2010
pubmed:articleTitle
IL-6 receptor-mediated lung Th2 cytokine networking in silica-induced pulmonary fibrosis.
pubmed:affiliation
Immunobiology Division, Indian Institute of Toxicology Research, Mahatma Gandhi Marg, Lucknow, 226001, India.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't