Linked Life Data

8821103

Source:http://linkedlifedata.com/resource/pubmed/id/8821103

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1996-11-6
pubmed:abstractText
Resolution of acute inflammation requires the removal of sequestered neutrophils (PMN) from the inflammatory site by apoptosis and ingestion by tissue macrophages; however, sequestered PMN are prevented from undergoing programmed cell death by some of the mediators of the acute inflammatory process, including lipopolysaccharide (LPS), granulocyte-macrophage colony-stimulating factor, and interleukin 2. This delay in apoptosis could lead to necrosis resulting in tissue damage. Tumor necrosis factor-alpha (TNF-alpha), Escherichia coli ingestion resulting in a respiratory burst, and heat have been shown to induce PMN apoptosis. The effects of TNF-alpha, E. coli ingestion, and heat shock on the one hand and LPS on the other, on PMN apoptosis are unknown. The aim of this study was to determine if TNF-alpha, E. coli ingestion, and heat shock, which have been shown to induce PMN apoptosis, could override the delay in apoptosis associated with LPS. PMN (10(6)) isolated from 10 healthy volunteers were cultured in either medium alone or PMN cultured with LPS (10 ng/mL/1 h). PMN activation was assessed subsequently by phagocytosis of E. coli and CD11b expression. PMN were then further studied under four culture conditions: medium alone, TNF-alpha (100 U/mL), E. coli (1:25, PMN:E. coli), and heat shock (42 degrees C for 45 min). Apoptosis was assessed over time by propidium iodide staining of DNA and Fc gamma RIII receptor expression. The results demonstrate, for the first time, that the mechanisms by which LPS delays PMN apoptosis are overridden by the mechanisms by which TNF-alpha, E. coli ingestion, and heat shock induce programmed cell death. Factors regulating PMN apoptosis have an important role to play in the resolution of acute inflammation. Identification of these factors and their interaction have important implications for the development of therapeutic strategies aimed at modulating the acute inflammatory response.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1073-2322
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
47-51
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Bacterial ingestion, tumor necrosis factor-alpha, and heat induce programmed cell death in activated neutrophils.
pubmed:affiliation
Department of Surgery, Royal College of Surgeons in Ireland, Dublin.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't