title: The expression and role of Fas ligand in intestinal inflammation.
abstract: Fas ligand (FasL) is involved in the pathogenesis of inflammatory diseases and immune privilege. We examined the expression of FasL in the enteric nervous system (ENS) in murine colitis and guinea-pig ileitis. We studied FasL immunoreactivity, functional integrity of the ENS, severity of colitis, and distribution of neutrophils in wild type and B6/gld mice that lack functional FasL. In ileitis, the distribution of FasL, CD4+ and CD8+ T cells was examined. FasL expression was increased in the ENS of wild type mice with colitis, but decreased labelling of nerve fibres was noted in B6/gld mice. Neutrophils were more abundant and widely distributed in B6/gld mice. Colitis was more severe and persistent in B6/gld mice 7 days after induction. Functional parameters of intestinal secretion and motility in B6/gld mice were the same as controls. In ileitis, FasL expression was increased in the guinea-pig ENS and returned to control levels following the resolution of inflammation. While T cells were not present in the ENS of controls, they were observed during inflammation, but were excluded from ganglia. The number of enteric neurons was unchanged over the course of inflammation. The expression of FasL is altered in intestinal inflammation and contributes to its resolution in experimental colitis.
authors.affiliation: Gastrointestinal Research Group, Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada. ksharkey@ucalgary.ca
authors.forename: F A
authors.initials: FA
authors.lastname: Sayani
authors.forename: C M
authors.initials: CM
authors.lastname: Keenan
authors.forename: M D
authors.initials: MD
authors.lastname: Van Sickle
authors.forename: K R
authors.initials: KR
authors.lastname: Amundson
authors.forename: E J
authors.initials: EJ
authors.lastname: Parr
authors.forename: R D
authors.initials: RD
authors.lastname: Mathison
authors.forename: W K
authors.initials: WK
authors.lastname: MacNaughton
authors.forename: J E A
authors.initials: JE
authors.lastname: Braun
authors.forename: K A
authors.initials: KA
authors.lastname: Sharkey
mesh_terms: D000818:Animals; D015153:Blotting, Western; D003092:Colitis / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism; D004195:Disease Models, Animal; D053222:Fas Ligand Protein; D005772:Gastrointestinal Transit / Q000502:physiology; D006168:Guinea Pigs; D007079:Ileitis / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism; D007150:Immunohistochemistry; D007249:Inflammation / Q000276:immunology / Q000378:metabolism*; D007422:Intestines / Q000502:physiology* / Q000503:physiopathology; D008297:Male; D008562:Membrane Glycoproteins / Q000096:biosynthesis*; D051379:Mice; D008822:Mice, Transgenic; D009197:Myenteric Plexus / Q000276:immunology / Q000378:metabolism*; D009504:Neutrophils / Q000276:immunology; D014302:Trinitrobenzenesulfonic Acid / Q000633:toxicity
chemical_list: D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D008562:Membrane Glycoproteins; D014302:Trinitrobenzenesulfonic Acid