Linked Life Data

8975870

Source:http://linkedlifedata.com/resource/pubmed/id/8975870

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1997-1-22
pubmed:abstractText
Activation of the microvasculature is a major component of the inflammatory response. During inflammation the vascular endothelium not only becomes more permeable to plasma proteins but also develops adhesion molecules that initiate the local immigration of leukocytes. We describe herein the in vivo changes in the three major vascular adhesion molecules during the development and healing of two types of rabbit dermal inflammatory lesions: (1) acute lesions produced in rabbits by the topical application of 1% sulfur mustard (SM, the military irritant/toxicant); and (2) chronic (immune-mediated) lesions produced in rabbits by intradermal injections of Mycobacterium bovis (BCG), the vaccine strain of tubercle bacillus. In each case, frozen tissue sections were made from lesions of various ages and stained immunohistochemically for von Willebrand (vW) factor to measure the total functional microvasculature. The sections were also stained immunohistochemically for the vascular endothelial adhesion molecules ICAM-1, ELAM-1 (E-selectin), and VCAM-1, and for the leukocyte ligands for ICAM-1: LFA-1 (CD11a/CD18) and Mac-1 (CD11b/CD18). Infiltrating monocytes and lymphocytes expressed the LFA-1 ligand and infiltrating PMN expressed the MAC-1 ligand. The area of stained microvasculature per square millimeter of tissue section was determined with the use of a computerized image analyzer. Edema and cell infiltration spread apart the microvessels, changing the number of microvessels per square millimeter of tissue section. Three methods of assessing such changes are presented. In SM lesions, endothelial ICAM levels were decreased from normal by about 50% at 1 and 2 days (when the lesions reached their peak size) and returned to normal at 3 and 6 days (during the healing process). ELAM rose in peak SM lesions and remained high during healing. VCAM levels, however, were only elevated in the 6-day (almost healed) lesions. In BCG lesions the levels of endothelial ICAM and VCAM (and to a lesser extent ELAM) were increased at 9 days and remained so as the size of the lesions peaked at 23 days. During the healing phase at 37 days, the elevated ICAM and VCAM levels decreased but the slightly increased ELAM levels persisted. These findings indicate that ELAM plays a major role in acute inflammation and that VCAM and ICAM play major roles in chronic inflammation. VCAM is known to be monocyte and lymphocyte selective.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0741-5400
pubmed:author
pubmed:issnType
Print
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
692-703
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8975870-Acute Disease, pubmed-meshheading:8975870-Animals, pubmed-meshheading:8975870-BCG Vaccine, pubmed-meshheading:8975870-Chronic Disease, pubmed-meshheading:8975870-E-Selectin, pubmed-meshheading:8975870-Endothelium, Vascular, pubmed-meshheading:8975870-Female, pubmed-meshheading:8975870-Hypersensitivity, Delayed, pubmed-meshheading:8975870-Inflammation, pubmed-meshheading:8975870-Intercellular Adhesion Molecule-1, pubmed-meshheading:8975870-Leukocyte Count, pubmed-meshheading:8975870-Leukocytes, Mononuclear, pubmed-meshheading:8975870-Lymphocyte Function-Associated Antigen-1, pubmed-meshheading:8975870-Mustard Gas, pubmed-meshheading:8975870-Neutrophils, pubmed-meshheading:8975870-Rabbits, pubmed-meshheading:8975870-Vascular Cell Adhesion Molecule-1, pubmed-meshheading:8975870-von Willebrand Factor
pubmed:year
1996
pubmed:articleTitle
Rabbit vascular endothelial adhesion molecules: ELAM-1 is most elevated in acute inflammation, whereas VCAM-1 and ICAM-1 predominate in chronic inflammation.
pubmed:affiliation
Department of Environmental Health Sciences, School of Hygiene and Public Health, The Johns Hopkins University, Baltimore, Maryland 21205, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.