Linked Life Data

15647285

Source:http://linkedlifedata.com/resource/pubmed/id/15647285

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
14
pubmed:dateCreated
2005-4-4
pubmed:databankReference
pubmed:abstractText
Pulmonary eosinophilia, a hallmark pathologic feature of allergic lung disease, is regulated by interleukin-13 (IL-13) as well as the eotaxin chemokines, but the specific role of these cytokines and their cooperative interaction are only partially understood. First, we elucidated the essential role of IL-13 in the induction of the eotaxins by comparing IL-13 gene-targeted mice with wild type control mice by using an ovalbumin-induced model of allergic airway inflammation. Notably, ovalbumin-induced expressions of eotaxin-1 and eotaxin-2 mRNA in the lungs were almost completely dependent upon IL-13. Second, in order to address the specific role of eotaxin-2 in IL-13-induced pulmonary eosinophilia, we generated eotaxin-2 gene-deficient mice by homologous recombination. Notably, in contrast to observations made in eotaxin-1-deficient mice, eotaxin-2-deficient mice had normal base-line eosinophil levels in the hematopoietic tissues and gastrointestinal tract. However, following intratracheal IL-13 administration, eotaxin-2-deficient mice showed a profound reduction in airway eosinophilia compared with wild type mice. Most interestingly, the level of peribronchial lung tissue eosinophils in IL-13-treated eotaxin-2-deficient mice was indistinguishable from wild type mice. Furthermore, IL-13 lung transgenic mice genetically engineered to be deficient in eotaxin-2 had a marked reduction of luminal eosinophils. Mechanistic analysis identified IL13-induced eotaxin-2 expression by macrophages in a distinct lung compartment (luminal inflammatory cells) compared with eotaxin-1, which was expressed solely in the tissue. Taken together, these results demonstrate a cooperative mechanism between IL-13 and eotaxin-2. In particular, IL-13 mediates allergen-induced eotaxin-2 expression, and eotaxin-2 mediates IL-13-induced airway eosinophilia.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
280
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
13952-61
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:15647285-Animals, pubmed-meshheading:15647285-Base Sequence, pubmed-meshheading:15647285-Bronchoalveolar Lavage Fluid, pubmed-meshheading:15647285-Chemokine CCL11, pubmed-meshheading:15647285-Chemokine CCL24, pubmed-meshheading:15647285-Chemokines, CC, pubmed-meshheading:15647285-Eosinophils, pubmed-meshheading:15647285-Gene Expression Regulation, pubmed-meshheading:15647285-Humans, pubmed-meshheading:15647285-In Situ Hybridization, pubmed-meshheading:15647285-Inflammation, pubmed-meshheading:15647285-Interleukin-13, pubmed-meshheading:15647285-Lung, pubmed-meshheading:15647285-Mice, pubmed-meshheading:15647285-Mice, Inbred BALB C, pubmed-meshheading:15647285-Mice, Inbred C57BL, pubmed-meshheading:15647285-Mice, Knockout, pubmed-meshheading:15647285-Molecular Sequence Data, pubmed-meshheading:15647285-Sequence Alignment, pubmed-meshheading:15647285-Tissue Distribution
pubmed:year
2005
pubmed:articleTitle
Identification of a cooperative mechanism involving interleukin-13 and eotaxin-2 in experimental allergic lung inflammation.
pubmed:affiliation
Division of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio 45229, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural