Linked Life Data

19385035

Source:http://linkedlifedata.com/resource/pubmed/id/19385035

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-4-21
pubmed:abstractText
The intense innate immunological activities occurring at the enteric mucosal surface involve interactions between intestinal epithelial cells and immune cells. Our previous studies have indicated that Peyer's patch lymphocytes may modulate intestinal epithelial barrier and ion transport function in homeostasis and host defense via cell-cell contact as well as cytokine signaling. The present study was undertaken using the established co-culture system of Caco-2 epithelial cells with lymphocytes of Peyer's patch to investigate the expression of IL-8 and IL-6 cytokines and cytokine receptors in the co-culture system after challenge with Shigella F2a-12 lipopolysaccharide (LPS). The human colonic epithelial cell line Caco-2 was co-cultured with freshly isolated lymphocytes from the murine Peyer's patch either in the mixed or separated (isolated but permeable compartments) co-culture configuration, and was challenged with Shigella F2a-12 LPS for 8 h. The level of mRNA expressions of human interleukin-8 (hIL-8), human interleukin-8 receptor (hIL-8R), mouse interleukin-8 receptor (mIL-8R), mouse interleukin-6 (mIL-6), mouse interleukin-6 receptor (mIL-6R) and human interleukin-6 receptor (hIL-6R) was examined by semi-quantitative PCR. In both co-culture groups, hIL-8 expression of Caco-2 cells was decreased, and hIL-8R expression was increased compared to the Caco-2 alone group. Upon LPS challenge, hIL-8 expression from the Caco-2 cells of both co-culture groups was higher than in the Caco-2 control group. The increased hIL-8 expression of Caco-2 cells in the separated co-culture group is correlated with a decreased hIL-8R expression and an increased mIL-8R expression. In the mixed co-culture group, the increased expression of hIL-8 was associated with the upregulated hIL-8R expression on Caco-2 cells and downregulated mIL-8R on murine Peyer's patch lymphocytes (PPL). mIL-6 expression from mouse PPL was also upregulated by LPS in mixed co-culture. However, upon the treatment with LPS, hIL-6R expression of Caco-2 cells was decreased in the mixed co-culture, but increased in separated co-culture. The data suggest that release of hIL-8 from epithelial cells may act on lymphocytes through a paracrine pathway, but it may also act on the epithelial cells themselves via an autocrine pathway. The data also suggest that the release of mIL-6 from Peyer's patch lymphocytes affects epithelial cells in a paracrine fashion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1095-8355
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
369-75
pubmed:meshHeading
pubmed-meshheading:19385035-Animals, pubmed-meshheading:19385035-Autocrine Communication, pubmed-meshheading:19385035-Caco-2 Cells, pubmed-meshheading:19385035-Cells, Cultured, pubmed-meshheading:19385035-Coculture Techniques, pubmed-meshheading:19385035-Epithelial Cells, pubmed-meshheading:19385035-Gene Expression Regulation, pubmed-meshheading:19385035-Humans, pubmed-meshheading:19385035-Interleukin-6, pubmed-meshheading:19385035-Interleukin-8, pubmed-meshheading:19385035-Intestinal Mucosa, pubmed-meshheading:19385035-Lipopolysaccharides, pubmed-meshheading:19385035-Lymphocytes, pubmed-meshheading:19385035-Mice, pubmed-meshheading:19385035-Paracrine Communication, pubmed-meshheading:19385035-Peyer's Patches, pubmed-meshheading:19385035-Receptors, Interleukin-6, pubmed-meshheading:19385035-Receptors, Interleukin-8
pubmed:year
2009
pubmed:articleTitle
Altered expression of inflammatory cytokine receptors in response to LPS challenge through interaction between intestinal epithelial cells and lymphocytes of Peyer's patch.
pubmed:affiliation
Epithelial Cell Biology Research Centre, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Department of Physiology, Shatin, Hong Kong.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't