Linked Life Data

11804871

Source:http://linkedlifedata.com/resource/pubmed/id/11804871

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-1-23
pubmed:abstractText
Airway inflammation and airway hyperresponsiveness (AHR) are hallmarks of asthma. Cytokines produced by T helper type 2 (Th2) lymphocytes have been implicated in both processes. There is strong support for the idea that Th2 cytokines can produce AHR indirectly by promoting the recruitment of inflammatory cells. Less attention has been given to the possibility that Th2 cytokines might induce AHR by acting directly on resident airway cells. To investigate this, we polarized and activated CD4(+) T cells in vitro and analyzed airway function after administration of lymphocyte-conditioned media to the airways of naive mice. Th2-lymphocyte-conditioned medium induced AHR within 6 h. This finding was reproduced in mast-cell-deficient and in T- and B-lymphocyte-deficient mice. AHR did not occur when Th2-lymphocyte-conditioned medium was administered to mice lacking the IL-4 receptor alpha subunit or Stat6, suggesting a critical role for interleukin (IL)-4 and/or IL-13. This was confirmed by the finding that recombinant IL-4 and IL-13 both induced AHR within 6 h. The induction of AHR occurred in the absence of inflammatory cell recruitment or mucus production. These results strongly suggest that products of activated Th2 lymphocytes can rapidly perturb airway function through direct effects on resident airway cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1044-1549
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
202-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11804871-Animals, pubmed-meshheading:11804871-Asthma, pubmed-meshheading:11804871-Bronchial Hyperreactivity, pubmed-meshheading:11804871-Bronchoalveolar Lavage Fluid, pubmed-meshheading:11804871-CD4-Positive T-Lymphocytes, pubmed-meshheading:11804871-Cells, Cultured, pubmed-meshheading:11804871-Culture Media, Conditioned, pubmed-meshheading:11804871-Epithelial Cells, pubmed-meshheading:11804871-Homeodomain Proteins, pubmed-meshheading:11804871-Humans, pubmed-meshheading:11804871-Interleukin-13, pubmed-meshheading:11804871-Interleukin-4, pubmed-meshheading:11804871-Lung, pubmed-meshheading:11804871-Lymphocyte Activation, pubmed-meshheading:11804871-Mast Cells, pubmed-meshheading:11804871-Mice, pubmed-meshheading:11804871-Mice, Inbred BALB C, pubmed-meshheading:11804871-Mice, Inbred C57BL, pubmed-meshheading:11804871-Receptors, Interleukin-4, pubmed-meshheading:11804871-Respiratory Mucosa, pubmed-meshheading:11804871-STAT6 Transcription Factor, pubmed-meshheading:11804871-Signal Transduction, pubmed-meshheading:11804871-Th2 Cells, pubmed-meshheading:11804871-Trans-Activators
pubmed:year
2002
pubmed:articleTitle
The Th2 lymphocyte products IL-4 and IL-13 rapidly induce airway hyperresponsiveness through direct effects on resident airway cells.
pubmed:affiliation
Lung Biology Center, Program in Immunology, University of California San Francisco, Box 0854, San Francisco, CA 94143-0854, USA. rvenk@itsa.ucsf.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't