title: Retinoic acid-inducible gene-I is constitutively expressed and involved in IFN-gamma-stimulated CXCL9-11 production in intestinal epithelial cells.
abstract: Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH/D family proteins, and plays an important role in antiviral response via interferon-stimulated genes (ISGs) and type 1 IFN. In this study, the roles of RIG-I in the epithelial cells in the cross-talk between type 2 IFN and inducible chemokines production are high-lighted. The results showed that RIG-I was constitutively expressed in normal surface epithelia lining the colonic mucosa. RIG-I was constitutively expressed in the epithelial cell lines HT-29, and IFN-gamma and TNF-alpha enhanced the RIG-I expression in a dose-dependent manner. IFN-gamma was shown to stimulate CXCL9-11 production, and RNA interference against RIG-I resulted in significant decrease of IFN-gamma-induced CXCL9-11 productions. These results suggest that RIG-I play an important role in the cross-talk between inflammatory cytokines and immune cell trafficking. In conclusion, RIG-I might regulate the gut barrier function in homeostatic and inflammatory conditions.
authors.affiliation: Department of Gastroenterology and Hematology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki, 036-8562, Japan. shogo.kawaguchi@gmail.com
authors.forename: Shogo
authors.initials: S
authors.lastname: Kawaguchi
authors.forename: Yoh
authors.initials: Y
authors.lastname: Ishiguro
authors.forename: Tadaatsu
authors.initials: T
authors.lastname: Imaizumi
authors.forename: Fumiaki
authors.initials: F
authors.lastname: Mori
authors.forename: Tomoh
authors.initials: T
authors.lastname: Matsumiya
authors.forename: Hidemi
authors.initials: H
authors.lastname: Yoshida
authors.forename: Ken
authors.initials: K
authors.lastname: Ota
authors.forename: Hirotake
authors.initials: H
authors.lastname: Sakuraba
authors.forename: Kazufumi
authors.initials: K
authors.lastname: Yamagata
authors.forename: Yuki
authors.initials: Y
authors.lastname: Sato
authors.forename: Kunikazu
authors.initials: K
authors.lastname: Tanji
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Haga
authors.forename: Koichi
authors.initials: K
authors.lastname: Wakabayashi
authors.forename: Shinsaku
authors.initials: S
authors.lastname: Fukuda
authors.forename: Kei
authors.initials: K
authors.lastname: Satoh
mesh_terms: D045744:Cell Line, Tumor; D054357:Chemokine CXCL10 / Q000096:biosynthesis* / Q000276:immunology; D054371:Chemokine CXCL11 / Q000096:biosynthesis* / Q000276:immunology; D054370:Chemokine CXCL9 / Q000096:biosynthesis*; D003110:Colonic Neoplasms / Q000276:immunology / Q000473:pathology; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases / Q000235:genetics*; D015870:Gene Expression; D019073:HT29 Cells; D006801:Humans; D007371:Interferon-gamma / Q000494:pharmacology; D007413:Intestinal Mucosa / Q000276:immunology; D007422:Intestines / Q000187:drug effects / Q000276:immunology* / Q000473:pathology; D034622:RNA Interference; D011971:Receptors, Immunologic; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D054357:Chemokine CXCL10; D054371:Chemokine CXCL11; D054370:Chemokine CXCL9; D011971:Receptors, Immunologic; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; C452820:RIGI protein, human; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases