PMID- 17034586
OWN - NLM
STAT- MEDLINE
DCOM- 20070117
LR  - 20240109
IS  - 0009-9104 (Print)
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Linking)
VI  - 146
IP  - 2
DP  - 2006 Nov
TI  - Interferon-gamma is causatively involved in experimental inflammatory bowel 
      disease in mice.
PG  - 330-8
AB  - Cytokines may be crucially involved in the pathogenesis of inflammatory bowel 
      diseases (IBD), but it remains controversial whether interferon (IFN)-gamma, a 
      typical proinflammatory cytokine, is an essential mediator to cause the 
      disorders. In the present study, IFN-gamma(-/-) and wild-type (WT) C57BL/6 mice 
      were fed 2.5% dextran sodium sulphate (DSS) in drinking water for 7 days, in 
      order to investigate DSS-induced intestinal inflammation. The DSS-treated WT mice 
      exhibited a robust production of IFN-gamma in the gut, a remarkable loss of body 
      weight, as well as high rate of mortality (60%). In striking contrast, IFN-gamma 
      deficient mice did not develop DSS-induced colitis, as indicated by the 
      maintenance of body weight and survival rate of 100%. Severe intestinal 
      inflammation was demonstrated exclusively in WT animals in terms of the 
      shortening of the bowel as well as the elevation of the disease activity index, 
      myeloperoxidase (MPO) activity and serum haptoglobin level. Histological study of 
      DSS-treated WT intestine revealed disruption of mucosal epithelium and massive 
      infiltration of inflammatory cells, while the organ from IFN-gamma(-/-) mice 
      remained virtually normal in appearance. Enzyme-linked immunosorbent assay 
      (ELISA) analyses indicated abundant production of three chemokines, i.e. monokine 
      induced by interferon-gamma (MIG), interferon-inducible protein 10 (IP-10) and 
      monocyte chemoattractant protein-1 (MCP-1), in the DSS-irritated intestine of WT 
      but not of IFN-gamma(-/-) mice. The present results demonstrate clearly that 
      IFN-gamma plays indispensable roles in the initiation of DSS colitis, and some 
      chemokines are produced in an IFN-gamma-dependent fashion.
FAU - Ito, R
AU  - Ito R
AD  - Department of Microbiology, Kyoto Prefectural University of Medicine, Kyoto, 
      Japan.
FAU - Shin-Ya, M
AU  - Shin-Ya M
FAU - Kishida, T
AU  - Kishida T
FAU - Urano, A
AU  - Urano A
FAU - Takada, R
AU  - Takada R
FAU - Sakagami, J
AU  - Sakagami J
FAU - Imanishi, J
AU  - Imanishi J
FAU - Kita, M
AU  - Kita M
FAU - Ueda, Y
AU  - Ueda Y
FAU - Iwakura, Y
AU  - Iwakura Y
FAU - Kataoka, K
AU  - Kataoka K
FAU - Okanoue, T
AU  - Okanoue T
FAU - Mazda, O
AU  - Mazda O
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CXCL10)
RN  - 0 (Chemokine CXCL9)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Cxcl9 protein, mouse)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 9042-14-2 (Dextran Sulfate)
RN  - EC 1.11.1.7 (Peroxidase)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Chemokine CCL2/biosynthesis
MH  - Chemokine CXCL10
MH  - Chemokine CXCL9
MH  - Chemokines, CXC/biosynthesis
MH  - Colitis/chemically induced/*immunology/pathology
MH  - Colon/immunology
MH  - Dextran Sulfate
MH  - Disease Models, Animal
MH  - Disease Susceptibility
MH  - Interferon-gamma/biosynthesis/deficiency/*immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Peroxidase/metabolism
MH  - Severity of Illness Index
MH  - Weight Loss
PMC - PMC1942055
EDAT- 2006/10/13 09:00
MHDA- 2007/01/18 09:00
PMCR- 2007/11/01
CRDT- 2006/10/13 09:00
PHST- 2006/10/13 09:00 [pubmed]
PHST- 2007/01/18 09:00 [medline]
PHST- 2006/10/13 09:00 [entrez]
PHST- 2007/11/01 00:00 [pmc-release]
AID - CEI3214 [pii]
AID - 10.1111/j.1365-2249.2006.03214.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2006 Nov;146(2):330-8. doi: 10.1111/j.1365-2249.2006.03214.x.