Linked Life Data

18453112

Source:http://linkedlifedata.com/resource/pubmed/id/18453112

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2008-5-5
pubmed:abstractText
Neutrophil-derived granule enzymes, oxidants, and mediators have been implicated in the pathogenesis of a variety of inflammatory diseases. Neutrophil apoptosis is associated with the loss of expression of adhesion molecules and greatly reduced responsiveness to external stimuli, so that these cells become functionally isolated from their environment. In contrast with necrosis, apoptosis is associated with preservation of plasma membrane integrity, so that release of harmful neutrophil contents is limited, and the inert neutrophils are phagocytosed by local macrophages. Furthermore, phagocytosis of apoptotic neutrophils by human macrophages in vitro suppresses release of macrophage-derived pro-inflammatory mediators. In this way, by downregulating neutrophil functions and triggering "silent" clearance by phagocytes, apoptosis provides a mechanism for the safe disposal of potentially destructive inflammatory cells. Many of the molecular events involved in the apoptosis pathway have been identified and several complementary methods may be employed to identify and quantitate neutrophil apoptosis. This chapter will discuss analysis of neutrophil morphology, DNA fragmentation, membrane changes, mitochondrial alterations, caspase activation, and phagocytosis of apoptotic neutrophils by macrophages.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1064-3745
pubmed:author
pubmed:issnType
Print
pubmed:volume
412
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
177-200
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Analysis of neutrophil apoptosis.
pubmed:affiliation
MRC/University of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh, United Kingdom.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't