| pubmed-article:8213996 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8213996 | lifeskim:mentions | umls-concept:C0027950 | lld:lifeskim |
| pubmed-article:8213996 | lifeskim:mentions | umls-concept:C0819757 | lld:lifeskim |
| pubmed-article:8213996 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:8213996 | lifeskim:mentions | umls-concept:C0449416 | lld:lifeskim |
| pubmed-article:8213996 | lifeskim:mentions | umls-concept:C0750502 | lld:lifeskim |
| pubmed-article:8213996 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:8213996 | pubmed:dateCreated | 1993-11-5 | lld:pubmed |
| pubmed-article:8213996 | pubmed:abstractText | The kinetic expression and potential cellular source of tumor necrosis factor-alpha (TNF-alpha) in lipopolysaccharide-(LPS) induced acute lung inflammation was investigated using a rat model by Northern blot analysis, in situ hybridization and immunohistochemistry. LPS induced a polymorphonuclear leukocyte infiltrate in the lung that peaked between 6 and 24 hours. TNF-alpha messenger (m)RNA was strongly induced by LPS in whole lung tissues shown by Northern analysis. Both alveolar macrophages and polymorphonuclear leukocytes (PMNs), purified from bronchoalveolar lavage fluids of LPS-treated rats, were shown to express TNF-alpha mRNA by Northern analysis. However, PMNs displayed several times more TNF-alpha mRNA, relative to actin mRNA, than alveolar macrophages at 6 and 12 hours. By in situ hybridization, most of the cells positive for TNF-alpha mRNA at 6 and 12 hours seemed to be PMNs located within the tissue near bronchioles or vessels. By immunohistochemistry, TNF-alpha protein was localized mainly to alveolar macrophages at early times (1 to 3 hours) after LPS challenge, and thereafter, PMNs seemed to be the predominant source of TNF-alpha protein as more than 90% of total intraalveolar positive cells at 6 and 12 hours were PMN. Thus, our data provide the first in vivo evidence that PMNs can serve as a significant source of TNF-alpha at sites of acute inflammation. | lld:pubmed |
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| pubmed-article:8213996 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8213996 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8213996 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:8213996 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8213996 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:8213996 | pubmed:issn | 0002-9440 | lld:pubmed |
| pubmed-article:8213996 | pubmed:author | pubmed-author:GauldieJJ | lld:pubmed |
| pubmed-article:8213996 | pubmed:author | pubmed-author:TorrePP | lld:pubmed |
| pubmed-article:8213996 | pubmed:author | pubmed-author:JordanaMM | lld:pubmed |
| pubmed-article:8213996 | pubmed:author | pubmed-author:KirpalaniHH | lld:pubmed |
| pubmed-article:8213996 | pubmed:author | pubmed-author:VegaE TET | lld:pubmed |
| pubmed-article:8213996 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8213996 | pubmed:volume | 143 | lld:pubmed |
| pubmed-article:8213996 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8213996 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8213996 | pubmed:pagination | 1009-15 | lld:pubmed |
| pubmed-article:8213996 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:8213996 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8213996 | pubmed:articleTitle | Polymorphonuclear leukocytes as a significant source of tumor necrosis factor-alpha in endotoxin-challenged lung tissue. | lld:pubmed |
| pubmed-article:8213996 | pubmed:affiliation | Department of Pathology, Chedoke-McMaster Medical Centre, McMaster University, Hamilton, Ontario, Canada. | lld:pubmed |
| pubmed-article:8213996 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8213996 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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