Linked Life Data

8610426

Source:http://linkedlifedata.com/resource/pubmed/id/8610426

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1996-5-29
pubmed:abstractText
A possible mechanism of the induction of lung transplant rejection by cytomegalovirus (CMV) infection is the inflammatory upregulation of adhesion ligand molecules on transplant endothelia by the viral infection leading to leukocyte activation. To study this question a rat model of rat cytomegalovirus (RCMV) infection and acute lung transplant rejection was established to study: (1) the influence of RCMV infection on the course of rejection, (2) the influence of rejection on the course of RCMV infection, and (3) the influence of RCMV on adhesion molecule expression and leukocyte infiltration. For this Lew (RT1l) rats received either syngenic (n=25) or allogeneic (BN, RT1n; n=38) left lateral lung transplants. Postoperatively, CsA 25mg/kg was given on days 1-3 and triple drug (CsA, Aza, Pred) immunosuppression was given from days 4-10 to induce systemic RCMV infection and acute rejection developed from postoperative day (POD) 15-25 in allogeneic transplants. In RCMV-positive animals the rejection grade was gradually increased at POD 15 and 18. Furthermore, after allogeneic transplantation an enhanced viral infection of the lung transplant as early as POD 11 was found and increased salivary gland PFU titers on days 20 and 25. In the absence of rejection infiltration a maximal induction of ICAM-1 adhesion molecules was found on lung endothelia in RCMV+ allogeneic animals as compared with noninfected controls. This induction was found to lesser degree for VCAM-1 and MHC class II adhesion ligand molecules. This was accompanied by a significantly increased CD11a+ and CD49d+ leukocyte infiltration into the alveolar interstitium on day 11 and 15 in infected transplants. The results show an enhancement of RCMV infection after allogeneic lung transplantation leading to endothelial activation and recruitment of CD11a/CD49d+ leukocytes. This mechanism may strongly influence transplant inflammation and the long-term course of lung transplant rejection.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0041-1337
pubmed:author
pubmed:issnType
Print
pubmed:day
27
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1250-60
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Enhancement of cytomegalovirus infection and acute rejection after allogeneic lung transplantation in the rat.
pubmed:affiliation
The Department of Cardiovascular Surgery, Christian Albrechts University, Kiel, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't