Source:http://linkedlifedata.com/resource/pubmed/id/14500663
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
|
| pubmed:dateCreated |
2003-9-22
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| pubmed:abstractText |
T helper 1 responses are typically proinflammatory, while Th2 responses have been considered regulatory. Interestingly, Th2 responses characterize a number of pulmonary diseases, many of which terminate in tissue remodeling and fibrosis. We developed a mouse model using Schistosoma mansoni eggs and cytokine-deficient mice to induce highly polarized Th1- or Th2-type inflammation in the lung. In this study, we examined the pathology and cytokine profiles in Th1- and Th2-polarized environments and used oligonucleotide microarray analysis to decipher the genes responsible for these effects. We further elaborated on the results using IL-10- and IL-13-deficient mice because these cytokines are believed to be the central regulators of Th2-associated pathology. We found that the Th1-polarized mice developed small granulomas with less fibrosis while expressing genes characteristic of tissue damage. Th2-polarized mice, in contrast, formed large granulomas with massive collagen deposition and up-regulated genes associated with wound healing, specifically, arginase, collagens, matrix metalloproteinases (MMPs), and tissue inhibitors of MMP. In addition, several members of the chitinase-like family were up-regulated in the lung following egg challenge. We also developed a method of defining the net collagen deposition using the expression profiles of several collagen, MMP, and tissue inhibitors of MMP genes. We found that Th1-polarized mice did not elaborate collagens or MMPs and therefore did not have a significant capacity for repair in this model. Thus, Th1-mediated inflammation is characterized by tissue damage, while Th2 directs wound healing and fibrosis.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Oct
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
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| pubmed:volume |
171
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
3655-67
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:14500663-Acute Disease,
pubmed-meshheading:14500663-Animals,
pubmed-meshheading:14500663-Antigens, Helminth,
pubmed-meshheading:14500663-Cells, Cultured,
pubmed-meshheading:14500663-Chitinase,
pubmed-meshheading:14500663-Cytokines,
pubmed-meshheading:14500663-Extracellular Matrix Proteins,
pubmed-meshheading:14500663-Gene Expression Profiling,
pubmed-meshheading:14500663-Immunophenotyping,
pubmed-meshheading:14500663-Lung Diseases, Parasitic,
pubmed-meshheading:14500663-Mice,
pubmed-meshheading:14500663-Mice, Inbred C57BL,
pubmed-meshheading:14500663-Mice, Knockout,
pubmed-meshheading:14500663-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:14500663-Ovum,
pubmed-meshheading:14500663-Schistosoma mansoni,
pubmed-meshheading:14500663-Schistosomiasis mansoni,
pubmed-meshheading:14500663-Species Specificity,
pubmed-meshheading:14500663-Th1 Cells,
pubmed-meshheading:14500663-Th2 Cells,
pubmed-meshheading:14500663-Up-Regulation,
pubmed-meshheading:14500663-Wound Healing
|
| pubmed:year |
2003
|
| pubmed:articleTitle |
Global gene expression profiles during acute pathogen-induced pulmonary inflammation reveal divergent roles for Th1 and Th2 responses in tissue repair.
|
| pubmed:affiliation |
Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
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| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|