title: Interleukin-5 participates in the pathogenesis of ileitis in SAMP1/Yit mice.
abstract: SAMP1/Yit mice spontaneously develop ileitis resembling Crohn's disease (CD) without chemical or genetic manipulations. Since the focus of studies were Th1 cytokines, only Th1-type T cells were thought to be responsible for intestinal inflammation in these mice. To further characterize the pathogenesis of this ileitis, we investigated the implication of Th2 cytokines in ileitis of SAMP1/Yit mice. The expression of chemokine receptors (CCR) associated with both Th1 and Th2 lymphocytes, such as CCR2, CCR3, CCR4, CCR5, and CCR8, was increased. Among cytokines, IL-5 was remarkably increased in Peyer's patches, mesenteric lymph nodes, and mucosa involved in ileitis. Furthermore, infiltration of numerous eosinophils in ileitis was histologically evident. Severe combined immunodeficiency mice injected intraperitoneally with CD4(+) cells from SAMP1/Yit mice developed colitis and ileitis, with the infiltration of eosinophils. Administration of anti-IL-5 antibodies significantly attenuated ileitis in these mice. We suggest that IL-5 participates in the pathogenesis of ileitis and that anti-IL-5 antibodies are potentially useful for immunotherapy in CD patients. This is the first demonstration that IL-5 is crucial for the development of ileitis in this mouse model of CD.
authors.affiliation: Second Department of Internal Medicine, Kurume University, Kurume, Fukuoka, Japan.
authors.forename: Hidetoshi
authors.initials: H
authors.lastname: Takedatsu
authors.forename: Keiichi
authors.initials: K
authors.lastname: Mitsuyama
authors.forename: Satoshi
authors.initials: S
authors.lastname: Matsumoto
authors.forename: Kazuyo
authors.initials: K
authors.lastname: Handa
authors.forename: Asuka
authors.initials: A
authors.lastname: Suzuki
authors.forename: Hiroko
authors.initials: H
authors.lastname: Takedatsu
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Funabashi
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Okabe
authors.forename: Taeko
authors.initials: T
authors.lastname: Hara
authors.forename: Atsushi
authors.initials: A
authors.lastname: Toyonaga
authors.forename: Michio
authors.initials: M
authors.lastname: Sata
mesh_terms: D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D003424:Crohn Disease / Q000276:immunology* / Q000473:pathology; D004195:Disease Models, Animal; D004804:Eosinophils / Q000276:immunology*; D005434:Flow Cytometry; D006651:Histocytochemistry; D007079:Ileitis / Q000276:immunology* / Q000473:pathology; D007082:Ileum / Q000276:immunology / Q000473:pathology; D016130:Immunophenotyping; D015848:Interleukin-5 / Q000235:genetics / Q000276:immunology*; D007413:Intestinal Mucosa / Q000276:immunology / Q000473:pathology; D051379:Mice; D016513:Mice, SCID; D012313:RNA / Q000737:chemistry / Q000235:genetics; D019707:Receptors, Chemokine / Q000235:genetics / Q000276:immunology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013047:Specific Pathogen-Free Organisms; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D015848:Interleukin-5; D019707:Receptors, Chemokine; D012313:RNA