Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2010-11-4
pubmed:abstractText
IL-33 is a member of the IL-1 family and mediates its biological effects via the ST2 receptor, which is selectively expressed on Th2 cells and mast cells. Although polymorphic variation in ST2 is strongly associated with asthma, it is currently unclear whether IL-33 acts directly on lung tissue cells at sites of airway remodeling. Therefore, we aimed to identify the IL-33-responsive cells among primary human lung tissue cells. ST2 mRNA was expressed in both endothelial and epithelial cells but not in fibroblasts or smooth muscle cells. Correspondingly, IL-33 promoted IL-8 production by both endothelial and epithelial cells but not by fibroblasts or smooth muscle cells. Transfection of ST2 small interference RNA into both endothelial and epithelial cells significantly reduced the IL-33-dependent upregulation of IL-8, suggesting that IL-33-mediated responses in these cells occur via the ST2 receptor. Importantly, Th2 cytokines, such as IL-4, further enhanced ST2 expression and function in both endothelial and epithelial cells. The IL-33-mediated production of IL-8 by epithelial cells was almost completely suppressed by corticosteroid treatment. In contrast, the effect of corticosteroid treatment on the IL-33-mediated responses of endothelial cells was only partial. IL-33 induced activation of both ERK and p38 MAPK in endothelial cells but only ERK in epithelial cells. p38 MAPK was required for the IL-33-mediated responses of endothelial cells, whereas ERK was required for IL-33-mediated IL-8 production by epithelial cells. Taken together, these findings suggest that IL-33-mediated inflammatory responses of lung tissue cells may be involved in the chronic allergic inflammation of the asthmatic airway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
185
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5743-50
pubmed:meshHeading
pubmed-meshheading:20926795-Asthma, pubmed-meshheading:20926795-Blotting, Western, pubmed-meshheading:20926795-Cells, Cultured, pubmed-meshheading:20926795-Endothelial Cells, pubmed-meshheading:20926795-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:20926795-Epithelial Cells, pubmed-meshheading:20926795-Fibroblasts, pubmed-meshheading:20926795-Humans, pubmed-meshheading:20926795-Inflammation, pubmed-meshheading:20926795-Interleukin-8, pubmed-meshheading:20926795-Interleukins, pubmed-meshheading:20926795-Lung, pubmed-meshheading:20926795-Myocytes, Smooth Muscle, pubmed-meshheading:20926795-RNA, Small Interfering, pubmed-meshheading:20926795-Receptors, Cell Surface, pubmed-meshheading:20926795-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:20926795-Signal Transduction, pubmed-meshheading:20926795-Transfection
pubmed:year
2010
pubmed:articleTitle
IL-33 mediates inflammatory responses in human lung tissue cells.
pubmed:affiliation
Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't