Dds in the treatment of inflammatory bowel disease

Toshifumi Hibi, Haruhiko Ogata

Research output: Contribution to journalArticle

Abstract

Inflammatory bowel disease (TBD) is thought to result from inappropriate activation of mucosal immune responses. Recently, further understanding the immunopathophysiology of IBD has provided more specific therapeutic approach such as new drug delivery systems using intestinal microflora, interleukin-7(IL-7)/IL-7R system or inducible-co-stimulator (ICOS) in mucosal T cells as a target for treatment of IBD. Administration of Lactococats lactis secreting interleukin 10 or antibody against ICOS molecule specifically expressed in the mucosal T cells of intestinal inflammation successfully treated the murine colitis. While it has been demonstrated that intesti nal epithelial cells produce IL-7 and that IL-7 serves as a regulatory factor for proliferation of mucosal lymphocytes expressing IL-7R. And intestinal epithelial cell-derived IL-7 plays a crucial role in the organization of mucosal lymphoid tissues and regulating the normal immune response in intestinal mucosa. In a previous study, IL-7 transgenic mice developed chronic colitis, and the essential role of mucosal IL-7/IL-7R-dependent signals was demonstrated in the development of chronic intestinal inflammation. These results indicate that mucosal IL-7/IL-7R-dependent signals are involved in the development of chronic intestinal inflammation in both the mouse model and human disease of the intestinal mucosa. Thus current studies indicate that therapeutic approaches by specific targeting of IL-7R-expressing mucosal T cells may be feasiblein the treatment of human IBD.

Original languageEnglish
Pages (from-to)84-89
Number of pages6
JournalDrug Delivery System
Volume19
Issue number2
DOIs
Publication statusPublished - 2004

Fingerprint

Interleukin-7
Inflammatory Bowel Diseases
Inducible T-Cell Co-Stimulator Protein
Colitis
Intestinal Mucosa
Inflammation
T-Lymphocytes
Therapeutics
Epithelial Cells
Mucosal Immunity
Lymphoid Tissue
Drug Delivery Systems
Interleukin-10
Transgenic Mice
Mucous Membrane
Lymphocytes
Antibodies

Keywords

  • Crohn's disease
  • gataulcerative colitis
  • inducible-co-stimulator
  • innate immunity
  • interleukin-7

ASJC Scopus subject areas

  • Pharmaceutical Science

Cite this

Dds in the treatment of inflammatory bowel disease. / Hibi, Toshifumi; Ogata, Haruhiko.

In: Drug Delivery System, Vol. 19, No. 2, 2004, p. 84-89.

Research output: Contribution to journalArticle

Hibi, Toshifumi ; Ogata, Haruhiko. / Dds in the treatment of inflammatory bowel disease. In: Drug Delivery System. 2004 ; Vol. 19, No. 2. pp. 84-89.
@article{0673106eb72f4f58b2eba9ac759b7812,
title = "Dds in the treatment of inflammatory bowel disease",
abstract = "Inflammatory bowel disease (TBD) is thought to result from inappropriate activation of mucosal immune responses. Recently, further understanding the immunopathophysiology of IBD has provided more specific therapeutic approach such as new drug delivery systems using intestinal microflora, interleukin-7(IL-7)/IL-7R system or inducible-co-stimulator (ICOS) in mucosal T cells as a target for treatment of IBD. Administration of Lactococats lactis secreting interleukin 10 or antibody against ICOS molecule specifically expressed in the mucosal T cells of intestinal inflammation successfully treated the murine colitis. While it has been demonstrated that intesti nal epithelial cells produce IL-7 and that IL-7 serves as a regulatory factor for proliferation of mucosal lymphocytes expressing IL-7R. And intestinal epithelial cell-derived IL-7 plays a crucial role in the organization of mucosal lymphoid tissues and regulating the normal immune response in intestinal mucosa. In a previous study, IL-7 transgenic mice developed chronic colitis, and the essential role of mucosal IL-7/IL-7R-dependent signals was demonstrated in the development of chronic intestinal inflammation. These results indicate that mucosal IL-7/IL-7R-dependent signals are involved in the development of chronic intestinal inflammation in both the mouse model and human disease of the intestinal mucosa. Thus current studies indicate that therapeutic approaches by specific targeting of IL-7R-expressing mucosal T cells may be feasiblein the treatment of human IBD.",
keywords = "Crohn's disease, gataulcerative colitis, inducible-co-stimulator, innate immunity, interleukin-7",
author = "Toshifumi Hibi and Haruhiko Ogata",
year = "2004",
doi = "10.2745/dds.19.84",
language = "English",
volume = "19",
pages = "84--89",
journal = "Drug Delivery System",
issn = "0913-5006",
publisher = "Japan Society of Drug Delivery System",
number = "2",

}

TY - JOUR

T1 - Dds in the treatment of inflammatory bowel disease

AU - Hibi, Toshifumi

AU - Ogata, Haruhiko

PY - 2004

Y1 - 2004

N2 - Inflammatory bowel disease (TBD) is thought to result from inappropriate activation of mucosal immune responses. Recently, further understanding the immunopathophysiology of IBD has provided more specific therapeutic approach such as new drug delivery systems using intestinal microflora, interleukin-7(IL-7)/IL-7R system or inducible-co-stimulator (ICOS) in mucosal T cells as a target for treatment of IBD. Administration of Lactococats lactis secreting interleukin 10 or antibody against ICOS molecule specifically expressed in the mucosal T cells of intestinal inflammation successfully treated the murine colitis. While it has been demonstrated that intesti nal epithelial cells produce IL-7 and that IL-7 serves as a regulatory factor for proliferation of mucosal lymphocytes expressing IL-7R. And intestinal epithelial cell-derived IL-7 plays a crucial role in the organization of mucosal lymphoid tissues and regulating the normal immune response in intestinal mucosa. In a previous study, IL-7 transgenic mice developed chronic colitis, and the essential role of mucosal IL-7/IL-7R-dependent signals was demonstrated in the development of chronic intestinal inflammation. These results indicate that mucosal IL-7/IL-7R-dependent signals are involved in the development of chronic intestinal inflammation in both the mouse model and human disease of the intestinal mucosa. Thus current studies indicate that therapeutic approaches by specific targeting of IL-7R-expressing mucosal T cells may be feasiblein the treatment of human IBD.

AB - Inflammatory bowel disease (TBD) is thought to result from inappropriate activation of mucosal immune responses. Recently, further understanding the immunopathophysiology of IBD has provided more specific therapeutic approach such as new drug delivery systems using intestinal microflora, interleukin-7(IL-7)/IL-7R system or inducible-co-stimulator (ICOS) in mucosal T cells as a target for treatment of IBD. Administration of Lactococats lactis secreting interleukin 10 or antibody against ICOS molecule specifically expressed in the mucosal T cells of intestinal inflammation successfully treated the murine colitis. While it has been demonstrated that intesti nal epithelial cells produce IL-7 and that IL-7 serves as a regulatory factor for proliferation of mucosal lymphocytes expressing IL-7R. And intestinal epithelial cell-derived IL-7 plays a crucial role in the organization of mucosal lymphoid tissues and regulating the normal immune response in intestinal mucosa. In a previous study, IL-7 transgenic mice developed chronic colitis, and the essential role of mucosal IL-7/IL-7R-dependent signals was demonstrated in the development of chronic intestinal inflammation. These results indicate that mucosal IL-7/IL-7R-dependent signals are involved in the development of chronic intestinal inflammation in both the mouse model and human disease of the intestinal mucosa. Thus current studies indicate that therapeutic approaches by specific targeting of IL-7R-expressing mucosal T cells may be feasiblein the treatment of human IBD.

KW - Crohn's disease

KW - gataulcerative colitis

KW - inducible-co-stimulator

KW - innate immunity

KW - interleukin-7

UR - http://www.scopus.com/inward/record.url?scp=85010186963&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85010186963&partnerID=8YFLogxK

U2 - 10.2745/dds.19.84

DO - 10.2745/dds.19.84

M3 - Article

VL - 19

SP - 84

EP - 89

JO - Drug Delivery System

JF - Drug Delivery System

SN - 0913-5006

IS - 2

ER -