NDLI: Intestinal expression of Fas and Fas ligand is upregulated by bacterial signaling through TLR4 and TLR5, with activation of Fas modulating intestinal TLR-mediated inflammation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	O'Donnell, Charlotte Lyons, Caitriona O'Brien, Stephen Brint, Elizabeth Keane, Jonathan Houston, Aileen Fernandes, Philana Fallon, Padraic Regan, Tim
Description	Author Affiliation: Fernandes P ( Department of Medicine, University College Cork, Cork, Ireland); O'Donnell C ( Department of Medicine, University College Cork, Cork, Ireland); Lyons C ( Department of Pathology, University College Cork, Cork, Ireland); Keane J ( Department of Pathology, University College Cork, Cork, Ireland); Regan T ( Department of Pathology, University College Cork, Cork, Ireland); O'Brien S ( Department of Pathology, University College Cork, Cork, Ireland); Fallon P ( Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland); Brint E ( Department of Pathology, University College Cork, Cork, Ireland); Houston A ( Department of Medicine, University College Cork, Cork, Ireland)
Abstract	TLRs play an important role in mediating intestinal inflammation and homeostasis. Fas is best studied in terms of its function in apoptosis, but recent studies demonstrate that Fas signaling may mediate additional functions such as inflammation. The role of Fas, and the Fas ligand (FasL), in the intestine is poorly understood. The aim of this study was to evaluate potential cross-talk between TLRs and Fas/FasL system in intestinal epithelial cells (IECs). IECs were stimulated with TLR ligands, and expression of Fas and FasL was investigated. Treatment with TLR4 and TLR5 ligands, but not TLR2 and 9 ligands, increased expression of Fas and FasL in IECs in vitro. Consistent with this finding, expression of intestinal Fas and FasL was reduced in vivo in the epithelium of TLR4 knockout (KO), 5KO, and germ-free mice, but not in TLR2KO mice. Modulating Fas signaling using agonistic anti-Fas augmented TLR4- and TLR5-mediated TNF- and IL-8 production by IECs. In addition, suppression of Fas in IECs reduced the ability of TLR4 and TLR5 ligands and the intestinal pathogens Salmonella typhimurium and Listeria monocytogenes to induce the expression of IL-8. In conclusion, this study demonstrates that extensive cross-talk in IECs occurs between the Fas and TLR signaling pathways, with the FasL/Fas system playing a role in TLR-mediated inflammatory responses in the intestine.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	12
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-12-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens, Cd95 Metabolism Fas Ligand Protein Inflammation Intestines Signal Transduction Toll-like Receptor 4 Toll-like Receptor 5 Animals Agonists Genetics Apoptosis Drug Effects Cell Line Cytokines Biosynthesis Disease Models, Animal Gene Expression Regulation Ht29 Cells Immunology Microbiology Intestinal Mucosa Ligands Listeria Monocytogenes Mice Mice, Knockout Nf-kappa B Phosphatidylinositol 3-kinases Salmonella Typhimurium Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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