Linked Life Data

7529801

Source:http://linkedlifedata.com/resource/pubmed/id/7529801

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1995-2-16
pubmed:abstractText
By using the model of acute injury caused by intrapulmonary deposition of IgG immune complexes, blocking mAb to CD11a, CD11b, L-selectin, and intercellular adhesion molecule-1 (ICAM-1) were administered either i.v. or intratracheally (i.t.). The effects of these interventions were assessed according to lung injury, lung content of myeloperoxidase (MPO), TNF-alpha, and cellular content in bronchoalveolar lavage (BAL) fluids, and up-regulation of pulmonary vascular ICAM-1. In animals treated i.v. with Abs to CD11a, L-selectin, or ICAM-1 lung injury was significantly attenuated in parallel with reduced lung content of MPO. Under similar conditions, treatment with anti-CD11b had no effect. However, when the same mAb were administered i.t., anti-CD11a and anti-L-selectin were without protective effects, whereas i.t. administered anti-CD11b and anti-ICAM-1 were each highly protective. The protective effects of anti-CD11b were related to profound reductions in BAL levels of TNF-alpha, pulmonary vascular up-regulation of ICAM-1, and lung content of MPO. The protective effects of i.t.-administered anti-ICAM-1 were not associated with reduced BAL levels of TNF-alpha. Protective effects of mAb were also reflected in reductions of retrievable neutrophils in BAL fluids. mAb to rat CD11b and CD18 but not to rat CD11a suppressed in vitro production of TNF-alpha by immune complex-stimulated rat alveolar macrophages. The mAb did not reduce NO2-/NO3- generation in stimulated macrophages but all mAb (except anti-ICAM-1) reduced O2- responses in macrophages. These data suggest a compartmentalized role for adhesion molecules in lung inflammatory injury after intraalveolar deposition of IgG immune complexes, with CD11a, L-selectin, and ICAM-1 being important in the vascular compartment for neutrophil recruitment, whereas in the alveolar compartment CD11b and ICAM-1 (but not CD11a and L-selectin) seem to play key roles.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
154
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1350-63
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:7529801-Alveolitis, Extrinsic Allergic, pubmed-meshheading:7529801-Animals, pubmed-meshheading:7529801-Antibodies, Monoclonal, pubmed-meshheading:7529801-Binding, Competitive, pubmed-meshheading:7529801-Bronchoalveolar Lavage Fluid, pubmed-meshheading:7529801-Cell Adhesion Molecules, pubmed-meshheading:7529801-Immune Complex Diseases, pubmed-meshheading:7529801-Injections, Intravenous, pubmed-meshheading:7529801-Intercellular Adhesion Molecule-1, pubmed-meshheading:7529801-Intubation, Intratracheal, pubmed-meshheading:7529801-L-Selectin, pubmed-meshheading:7529801-Lymphocyte Function-Associated Antigen-1, pubmed-meshheading:7529801-Macrophage-1 Antigen, pubmed-meshheading:7529801-Macrophages, Alveolar, pubmed-meshheading:7529801-Rats, pubmed-meshheading:7529801-Reactive Oxygen Species, pubmed-meshheading:7529801-Receptors, Leukocyte-Adhesion, pubmed-meshheading:7529801-Tumor Necrosis Factor-alpha
pubmed:year
1995
pubmed:articleTitle
Compartmentalized roles for leukocytic adhesion molecules in lung inflammatory injury.
pubmed:affiliation
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.