Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2010-2-18
pubmed:abstractText
CCL3 is a protein of the CC chemokine family known to be important for T cell recruitment in inflammatory diseases. The aim of the current study was to evaluate the effects and putative mechanism of action of evasin-1, a novel CCL3-binding protein, in the pathogenesis of acute graft-versus-host disease (GVHD). GVHD was induced by the transplantation of splenocytes from C57BL/6J to B6D2F1 mice. Treatment of recipient mice with evasin-1 prevented mortality associated with GVHD. This was correlated with reduced weight loss and clinical disease severity. Analysis of the small intestine showed that evasin-1 treatment reduced the histopathological score and decreased levels of IFN-gamma and CCL5. Mechanistically, evasin-1 treatment reduced the number of CD4(+) and CD8(+) T cells infiltrating the small intestine, as assessed by immunohistochemistry, and the adhesion of leukocytes to intestinal venules of recipient mice, as assessed by intravital microscopy. Evasin-1 was also able to decrease liver damage, as seen by reduction of inflammatory infiltrate and IFN-gamma levels. Treatment with evasin-1 did not interfere with graft-versus-leukemia. Altogether, our studies demonstrate that CCL3 plays a major role in mediating GVHD, but not graft-versus-leukemia in mice and suggest that blockade of CCL3 with evasin-1 has potential therapeutic application in patients undergoing bone marrow transplantation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
184
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2646-54
pubmed:meshHeading
pubmed-meshheading:20100934-Animals, pubmed-meshheading:20100934-Anti-Inflammatory Agents, pubmed-meshheading:20100934-CD4-Positive T-Lymphocytes, pubmed-meshheading:20100934-CD8-Positive T-Lymphocytes, pubmed-meshheading:20100934-Cell Transplantation, pubmed-meshheading:20100934-Chemokine CCL3, pubmed-meshheading:20100934-Chemokine CCL5, pubmed-meshheading:20100934-Dexamethasone, pubmed-meshheading:20100934-Female, pubmed-meshheading:20100934-Graft vs Host Disease, pubmed-meshheading:20100934-Graft vs Leukemia Effect, pubmed-meshheading:20100934-Immunohistochemistry, pubmed-meshheading:20100934-Interferon-gamma, pubmed-meshheading:20100934-Intestine, Small, pubmed-meshheading:20100934-Macrophage Inflammatory Proteins, pubmed-meshheading:20100934-Male, pubmed-meshheading:20100934-Mice, pubmed-meshheading:20100934-Mice, Inbred C57BL, pubmed-meshheading:20100934-Mice, Inbred DBA, pubmed-meshheading:20100934-Mice, Inbred Strains, pubmed-meshheading:20100934-Mice, Transgenic, pubmed-meshheading:20100934-Receptors, Chemokine, pubmed-meshheading:20100934-Spleen
pubmed:year
2010
pubmed:articleTitle
The CCL3/macrophage inflammatory protein-1alpha-binding protein evasin-1 protects from graft-versus-host disease but does not modify graft-versus-leukemia in mice.
pubmed:affiliation
Laboratório de Imunofarmacologia, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, BeloHorizonte, Brazil.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't