Linked Life Data

21225224

Source:http://linkedlifedata.com/resource/pubmed/id/21225224

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2011-1-26
pubmed:abstractText
Autophagy is an evolutionarily conserved process that maintains cellular homeostasis via synthesis, degradation, and subsequent recycling of cellular products under various physiological conditions. However, the link between autophagy and the innate immune system remains unknown. In the present study, we evaluated Toll-like receptor (TLR)-mediated autophagy induction in intestinal epithelial cells (IECs) and its relationship to interleukin (IL)-8 production. IEC-6, HCT-15, RAW264.7, and THP-1 cells were cultured with or without various TLR ligands, followed by evaluation of the expressions of pro-inflammatory cytokines [IL-8, cytokine-induced neutrophil chemoattractants (CINC)-2?, macrophage inflammatory protein (MIP)-2] by real-time PCR and ELISA. To reveal the status of autophagy in IECs and macrophages, light chain 3 (LC3)-II expression was examined using Western blotting and immunofluorescence with confocal microscopy. Also, to evaluate the influence of TLR ligands on autophagy-mediated innate-immune responses, autophagy-related gene (Atg)7 specific siRNA was transfected into intestinal epithelial cells and IL-8 expression was determined following exposure to various TLR ligands. Cells treated with the TLR ligands produced considerable amounts of pro-inflammatory cytokines (IL-8, CINC-2?, MIP-2). Furthermore, the basal levels of LC3-II were markedly higher in IECs as compared to those in macrophages. Our findings indicated that autophagy induction following TLR ligand stimulation was not significantly evident in IECs as compared to macrophages. In addition, Atg7 gene expression silencingled to down-regulation of TLR-mediated IL-8 expression in IECs, which indicates a potential role of autophagy in generating innate-immune responses. In conclusion, autophagy may be an important intracellular machinery for inducing the innate immune system in IECs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Atg7 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Atg7 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL2, http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CXC, http://linkedlifedata.com/resource/pubmed/chemical/Cxcl2 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Cxcl2 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Gm1960 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/IL8 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8, http://linkedlifedata.com/resource/pubmed/chemical/Microtubule-Associated Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors, http://linkedlifedata.com/resource/pubmed/chemical/Ubiquitin-Activating Enzymes
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1791-244X
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
337-44
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Autophagy is required for toll-like receptor-mediated interleukin-8 production in intestinal epithelial cells.
pubmed:affiliation
Department of Internal Medicine II, Shimane University School of Medicine, Izumo, Shimane, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't