Linked Life Data

9761755

Source:http://linkedlifedata.com/resource/pubmed/id/9761755

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1998-11-5
pubmed:abstractText
A pulmonary Cryptococcus neoformans (Cne: strain 52D, ATCC24067) infection model in mice was used to examine the possible role for T cell-mediated immunity in regulating vascular adhesion molecules on lung endothelium during development of granulomatous inflammation. Resolution of pulmonary Cne infection in C.B-17 mice begins by Day 14 following intratracheal inoculation and depends on T cell-mediated recruitment of monocytes followed by their activation. C.B-17 scid/scid (SCID) mice mount a less exuberant pulmonary inflammatory response, recruit fewer monocytes into their lungs, and fail to clear the infection. Recruitment of leukocytes into infected tissue is mediated by both the interaction of adhesion molecules expressed on the surface of activated vascular endothelial cells with ligands on circulating cells, and the directed response of these leukocytes to chemotactic factors. The kinetics of expression of the endothelial cell adhesion molecules E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), all previously shown to regulate monocyte recruitment, were examined in the lungs of infected C.B-17 and SCID mice during pulmonary infection to determine if T cells were necessary for their upregulation. Immunohistochemical analysis showed that upregulation of E-selectin, VCAM-1, and ICAM-1 did not differ significantly between C.B-17 and SCID mice at any time during infection. Maximal expression in C.B-17 and SCID mice was noted between Days 5 and 7 for all three molecules and preceded maximal influx of leukocytes into the lung. Thus, the inability of SCID mice to recruit optimal numbers of monocytes into infected lungs was not the result of a failure to express the critical adhesion molecules early in infection, but likely reflected absence of immune dependent chemotactic factors.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1044-1549
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
588-97
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
T and B cell independence of endothelial cell adhesion molecule expression in pulmonary granulomatous inflammation.
pubmed:affiliation
Department of Microbiology, Midwestern University, Downers Grove, Illinois, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.