Linked Life Data

1347308

Source:http://linkedlifedata.com/resource/pubmed/id/1347308

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1992-4-9
pubmed:abstractText
The roles of beta 2 integrin molecules in neutrophil accumulation and tissue injury have been examined by the use of antibodies that are reactive with human CD11b and CD18 and cross-react with the homologous epitopes on rat neutrophils. Adherence to rat pulmonary artery endothelial cells by human neutrophils and endothelial cell killing by phorbol ester-activated human neutrophils required CD11b, CD11c, and CD18. Companion adherence studies between rat neutrophils and endothelial cells revealed a requirement for both CD11b and CD18. Neither anti-CD11b nor anti-CD18 depressed in vitro responses (O2- generation and chemotactic migration) of rat neutrophils. The accumulation of neutrophils in glycogen-induced peritoneal exudates was diminished substantially in rats treated with either anti-CD18 or anti-CD11b. In oxidant-mediated acute lung injury induced by rapid intravascular infusion of cobra venom factor, treatment of rats with either anti-CD18 or anti-CD11b significantly attenuated injury as assessed by increases in vascular permeability and hemorrhage. These protective effects correlated morphologically with diminished adhesion of neutrophils to interstitial intrapulmonary capillary endothelial cells. In studies of immune complex (BSA-anti-BSA)-induced alveolitis and dermal vasculitis, anti-CD18 had protective effects at all doses of anti-BSA employed. The protective effects of anti-CD18 correlated with diminished neutrophil accumulation in tissues at lower doses of anti-BSA. Although anti-CD11b was not effective under the same experimental conditions, intratracheal administration of this antibody conveyed protection against immune complex-induced lung injury, suggesting that both CD11b and CD18 are required for the full expression of injury. The current studies also demonstrated that when surface-bound IgG immune complexes were treated with fresh rat serum, the increment in O2- and TNF alpha generated by alveolar macrophages was suppressed by anti-CD18, but not by anti-CD11b, suggesting a heretofore unrecognized role for CD18 in the O2- and TNF-alpha responses of alveolar macrophages. Thus, neutrophil beta 2 integrins play a requisite role for the full expression of complement-dependent and oxygen radical-mediated injury of the lung and dermal vasculature.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
148
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1847-57
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:1347308-Animals, pubmed-meshheading:1347308-Antigen-Antibody Complex, pubmed-meshheading:1347308-Antigens, CD, pubmed-meshheading:1347308-Antigens, CD11, pubmed-meshheading:1347308-Antigens, CD18, pubmed-meshheading:1347308-Cell Adhesion, pubmed-meshheading:1347308-Complement Activation, pubmed-meshheading:1347308-Cytotoxicity, Immunologic, pubmed-meshheading:1347308-Free Radicals, pubmed-meshheading:1347308-Inflammation, pubmed-meshheading:1347308-Integrins, pubmed-meshheading:1347308-Lung, pubmed-meshheading:1347308-Macrophages, Alveolar, pubmed-meshheading:1347308-Neutrophils, pubmed-meshheading:1347308-Peroxidase, pubmed-meshheading:1347308-Rats, pubmed-meshheading:1347308-Respiratory Burst, pubmed-meshheading:1347308-Skin, pubmed-meshheading:1347308-Superoxides, pubmed-meshheading:1347308-Tumor Necrosis Factor-alpha
pubmed:year
1992
pubmed:articleTitle
Roles of beta 2 integrins of rat neutrophils in complement- and oxygen radical-mediated acute 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., Research Support, Non-U.S. Gov't