Linked Life Data

9047380

Source:http://linkedlifedata.com/resource/pubmed/id/9047380

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
14
pubmed:dateCreated
1997-3-20
pubmed:abstractText
Multiple organ dysfunction syndrome (MODS) is a major cause of morbidity and mortality in surgical intensive care units. It is characterized by progressive failure of two or more organs remote from the origin of injury. Since MODS results from a severe generalized inflammatory response, both chemokines and complement have had a proposed role in its pathophysiology. The availability of macrophage inflammatory protein 1 alpha (MIP-1alpha) knockout mice and congenic C5-deficient and C5-sufficient mice allowed us to investigate the individual contribution of these immune modulators in MODS. It has been demonstrated in this assay that MIP-1alpha has a protective role against MODS mortality, while C5a contributes to MODS mortality. Using a zymosan-induced MODS murine model, the absence of MIP-1alpha increased mortality four-fold, whereas the absence of C5 decreased mortality four-fold. Therefore, MIP-1alpha-dependent mediators are essential in the prevention of MODS related deaths, while C5-dependent mediators of inflammation can be considered to be contributing to the development of MODS related deaths.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0161-5890
pubmed:author
pubmed:issnType
Print
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1135-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Two chemotactic factors, C5a and MIP-1alpha, dramatically alter the mortality from zymosan-induced multiple organ dysfunction syndrome (MODS): C5a contributes to MODS while MIP-1alpha has a protective role.
pubmed:affiliation
Department of Microbiology and Immunology, University of Louisville, School of Medicine, KY 40292, U.S.A.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't