Linked Life Data

11159016

Source:http://linkedlifedata.com/resource/pubmed/id/11159016

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-2-22
pubmed:abstractText
Intratracheal administration of interleukin-10 (IL-10) has been reported to inhibit allergic inflammation but augment airway hyperresponsiveness (AHR). In the present study, airway and smooth muscle responsiveness to methacholine (MCh) were compared in wild-type (WT) and IL-10-deficient (IL-10-KO) mice to investigate the role of endogenous IL-10 in AHR development. Naive WT and IL-10-KO mice exhibited similar dose-dependent increases in airway resistance (Raw) to intravenous MCh. Sensitization and challenge with ragweed (RW) induced a twofold increase in responsiveness to intravenous MCh in WT mice, but hyperresponsiveness was not observed in similarly treated IL-10-KO mice. Likewise, tracheal rings from RW-sensitized and -challenged WT mice exhibited a fourfold greater responsiveness to MCh than IL-10-KO tracheal preparations. Measurements of airway constriction by whole body plethysmography further supported the Raw and tracheal ring data (i.e., AHR was not observed in the absence of IL-10). Interestingly, factors previously implicated in the development of AHR, including IL-4, IL-5, IL-13, IgA, IgG1, IgE, eosinophilia, and lymphocyte recruitment to the airways, were upregulated in the IL-10-KO mice. Treatment with recombinant murine IL-10 at the time of allergen challenge reduced the magnitude of inflammation but reinstated AHR development in IL-10-KO mice. Adoptive transfer of mononuclear splenocytes to IL-10-sufficient severe combined immunodeficient mice indicated that lymphocytes were an important source of the IL-10 impacting AHR development. These results provide evidence that IL-10 expression promotes the development of allergen-induced smooth muscle hyperresponsiveness.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1040-0605
pubmed:author
pubmed:issnType
Print
pubmed:volume
280
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
L363-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11159016-Adoptive Transfer, pubmed-meshheading:11159016-Allergens, pubmed-meshheading:11159016-Animals, pubmed-meshheading:11159016-Bronchial Provocation Tests, pubmed-meshheading:11159016-Bronchoalveolar Lavage Fluid, pubmed-meshheading:11159016-Dose-Response Relationship, Drug, pubmed-meshheading:11159016-Immunoglobulins, pubmed-meshheading:11159016-Inflammation, pubmed-meshheading:11159016-Interleukin-10, pubmed-meshheading:11159016-Interleukin-13, pubmed-meshheading:11159016-Interleukin-4, pubmed-meshheading:11159016-Interleukin-5, pubmed-meshheading:11159016-Male, pubmed-meshheading:11159016-Methacholine Chloride, pubmed-meshheading:11159016-Mice, pubmed-meshheading:11159016-Mice, Inbred C57BL, pubmed-meshheading:11159016-Mice, Knockout, pubmed-meshheading:11159016-Mice, SCID, pubmed-meshheading:11159016-Recombinant Proteins, pubmed-meshheading:11159016-Respiratory Hypersensitivity, pubmed-meshheading:11159016-Spleen, pubmed-meshheading:11159016-Th2 Cells
pubmed:year
2001
pubmed:articleTitle
IL-10 gene knockout attenuates allergen-induced airway hyperresponsiveness in C57BL/6 mice.
pubmed:affiliation
Departments of Physiology and Pharmacology, Brody School of Medicine at East Carolina University, Greenville, North Carolina 27858, USA.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't