Linked Life Data

11034416

Source:http://linkedlifedata.com/resource/pubmed/id/11034416

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2000-10-16
pubmed:abstractText
Chronic Th2-dominated inflammation and exaggerated IL-6 production are characteristic features of the asthmatic airway. To understand the processes that are responsible for the chronicity of this response and the role(s) of IL-6 in the regulation of airway Th2 inflammation, we compared the responses induced by OVA in sensitized wild-type mice, IL-6 deficient (-/-) mice, and transgenic mice in which IL-6 was overexpressed in the airway (CC10-IL-6 mice). When compared with wild-type mice, IL-6-/- mice manifest exaggerated inflammation and eosinophilia, increased levels of IL-4, IL-5, and IL-13 protein and mRNA, exaggerated levels of eotaxin, JE/monocyte chemoattractant protein-1, macrophage inflammatory protein-1alpha and -2, and mRNA, increased bronchoalveolar lavage (BAL) TGF-beta1, and exaggerated airway responses to aerosolized methacholine. In contrast, CC10-IL-6 mice, on both C57BL/6 and BALB/c backgrounds, manifest diminished inflammation and eosinophilia, decreased levels of IL-4, IL-5, and IL-13 protein and mRNA, and decreased levels of bronchoalveolar lavage TGF-beta1. IL-6 also decreased the expression of endothelial VCAM-1 and airway responsiveness to methacholine in these animals. These alterations in the IL-6-/- and CC10-IL-6 mice were not associated with significant decreases or increases in the levels of IFN-gamma, respectively. These studies demonstrate that endogenous and exogenous IL-6 inhibit aeroallergen-induced Th2 inflammation and that this inhibition is not mediated by regulatory effects of IFN-gamma. IL-6 may be an important anti-inflammatory, counterregulatory, and healing cytokine in the airway.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
165
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4051-61
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11034416-Administration, Intranasal, pubmed-meshheading:11034416-Aerosols, pubmed-meshheading:11034416-Allergens, pubmed-meshheading:11034416-Animals, pubmed-meshheading:11034416-Bronchial Hyperreactivity, pubmed-meshheading:11034416-Chemokines, pubmed-meshheading:11034416-Cytokines, pubmed-meshheading:11034416-Gene Expression Regulation, pubmed-meshheading:11034416-Inflammation, pubmed-meshheading:11034416-Interleukin-6, pubmed-meshheading:11034416-Lung, pubmed-meshheading:11034416-Mice, pubmed-meshheading:11034416-Mice, Inbred BALB C, pubmed-meshheading:11034416-Mice, Inbred C57BL, pubmed-meshheading:11034416-Mice, Inbred CBA, pubmed-meshheading:11034416-Mice, Knockout, pubmed-meshheading:11034416-Mice, Transgenic, pubmed-meshheading:11034416-Ovalbumin, pubmed-meshheading:11034416-Plethysmography, Whole Body, pubmed-meshheading:11034416-Pulmonary Eosinophilia, pubmed-meshheading:11034416-RNA, Messenger, pubmed-meshheading:11034416-Th2 Cells, pubmed-meshheading:11034416-Vascular Cell Adhesion Molecule-1
pubmed:year
2000
pubmed:articleTitle
Endogenous and exogenous IL-6 inhibit aeroallergen-induced Th2 inflammation.
pubmed:affiliation
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.