Linked Life Data

11160340

Source:http://linkedlifedata.com/resource/pubmed/id/11160340

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2001-2-22
pubmed:abstractText
Bronchial-alveolar eosinophilic inflammation is among the characteristic pathological changes in asthma, which has been shown to be correlated with type 2 cytokine and chemokine production. Exogenous IL-12 has been found to be inhibitory for pulmonary eosinophilia in reported studies. Using a murine asthma-like model induced by OVA, we found in the present study that IL-12 gene knockout (KO) mice showed substantially reduced airway recruitment of eosinophils compared with wild-type control mice following OVA sensitization/challenge, although the levels of circulating eosinophils were comparable in these two groups of mice. Cytokine analysis showed Ag-driven Th1 (IFN-gamma) and Th2 (IL-4, IL-5, IL-10, and IL-13) cytokine production by CD4 T cells from local draining lymph nodes and spleen. Similarly, local eotaxin production was comparable in wild-type and IL-12 KO mice. In contrast, immunohistochemical analysis showed that the expression of VCAM-1 on the lung endothelium of IL-12 KO mice was dramatically less than that in wild-type mice. Furthermore, administration of rIL-12 at the stage of sensitization and challenge with OVA restored airway eosinophilia and VCAM-1 expression in IL-12 KO mice. The results suggest that endogenous IL-12 contributes to the recruitment of eosinophils into airways observed in asthma, possibly via enhancement of the expression of VCAM-1 on local vascular endothelial cells.
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
15
pubmed:volume
166
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2741-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11160340-Administration, Intranasal, pubmed-meshheading:11160340-Animals, pubmed-meshheading:11160340-Asthma, pubmed-meshheading:11160340-Bronchi, pubmed-meshheading:11160340-Cytokines, pubmed-meshheading:11160340-Disease Models, Animal, pubmed-meshheading:11160340-Down-Regulation, pubmed-meshheading:11160340-Endothelium, Vascular, pubmed-meshheading:11160340-Female, pubmed-meshheading:11160340-Immunoglobulin E, pubmed-meshheading:11160340-Immunoglobulin G, pubmed-meshheading:11160340-Injections, Intraperitoneal, pubmed-meshheading:11160340-Interleukin-12, pubmed-meshheading:11160340-Intracellular Fluid, pubmed-meshheading:11160340-Mice, pubmed-meshheading:11160340-Mice, Inbred C57BL, pubmed-meshheading:11160340-Mice, Knockout, pubmed-meshheading:11160340-Mycobacterium bovis, pubmed-meshheading:11160340-Ovalbumin, pubmed-meshheading:11160340-Pulmonary Eosinophilia, pubmed-meshheading:11160340-Recombinant Proteins, pubmed-meshheading:11160340-Th1 Cells, pubmed-meshheading:11160340-Th2 Cells, pubmed-meshheading:11160340-Tuberculosis, Pulmonary, pubmed-meshheading:11160340-Vascular Cell Adhesion Molecule-1
pubmed:year
2001
pubmed:articleTitle
IL-12-dependent vascular cell adhesion molecule-1 expression contributes to airway eosinophilic inflammation in a mouse model of asthma-like reaction.
pubmed:affiliation
Immune Regulation of Allergy Research Group, Departments of Medical Microbiology and Immunology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't