PMID- 17016619
OWN - NLM
STAT- MEDLINE
DCOM- 20070109
LR  - 20130118
IS  - 1107-3756 (Print)
IS  - 1107-3756 (Linking)
VI  - 18
IP  - 5
DP  - 2006 Nov
TI  - Suppressive effect of non-anaphylactogenic anti-IgE antibody on the development 
      of dextran sulfate sodium-induced colitis.
PG  - 893-9
AB  - Inflammatory bowel disease (IBD) is a spectrum of immune-mediated chronic 
      disorders of the intestine. Patients with IBD tend to exhibit significantly 
      elevated levels of IgE in their serum. In general, the pathogenesis of IBD 
      exhibits inflammatory events such as immunoglobulin E (IgE)-mediated 
      hypersensitivity. We examined the effect of the non-anaphylactogenic anti-IgE 
      antibody, which has been known to block IgE functions, in an animal model of 
      ulcerative colitis induced by the oral intake of dextran sulfate sodium (DSS) for 
      seven days. The non-anaphylactogenic anti-IgE antibody was subcutaneously 
      injected on day 0 of DSS treatment. The disease activity index (DAI) was 
      calculated by scoring intestinal states, including body weight loss, diarrhea, 
      and rectal bleeding, and the activities of myeloperoxidase (MPO) and chymase were 
      measured in the colon tissue. In addition, the expression of tumor necrosis 
      factor (TNF)-alpha and cyclooxygenase (COX)-2 was determined by Western blotting. 
      Administration of the anti-IgE antibody markedly reduced the histological damage 
      to the colon and the DAI increment exhibited by the DSS-induced colitis. The 
      anti-IgE antibody also significantly suppressed the activities of MPO and chymase 
      as well as the expression of TNF-alpha and COX-2 in the DSS-treated colon tissue. 
      Furthermore, the elevation of IgE levels in serum was induced by DSS and reduced 
      by anti-IgE antibody injection. Thus, these results indicate that the IgE 
      response played an important role in the clinical signs and the expression of 
      inflammatory mediators in a colitis model caused by DSS treatment, suggesting 
      that the non-anaphylactogenic anti-IgE antibody may be a useful therapeutic agent 
      for ulcerative colitis.
FAU - Kang, Ok-Hwa
AU  - Kang OH
AD  - Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University, 
      Jeonbuk 570-749, Korea.
FAU - Kim, Dae-Ki
AU  - Kim DK
FAU - Choi, Yeon-A
AU  - Choi YA
FAU - Park, Hye-Jung
AU  - Park HJ
FAU - Tae, Jin
AU  - Tae J
FAU - Kang, Chon-Sik
AU  - Kang CS
FAU - Choi, Suck-Chei
AU  - Choi SC
FAU - Nah, Yong-Ho
AU  - Nah YH
FAU - Lee, Hern-Ku
AU  - Lee HK
FAU - Lee, Young-Mi
AU  - Lee YM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (Antibodies, Anti-Idiotypic)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (anti-IgE antibodies)
RN  - 9042-14-2 (Dextran Sulfate)
RN  - EC 1.11.1.7 (Peroxidase)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 3.4.21.39 (Chymases)
SB  - IM
MH  - Anaphylaxis/immunology
MH  - Animals
MH  - Antibodies, Anti-Idiotypic/*therapeutic use
MH  - Chymases/metabolism
MH  - Colitis, Ulcerative/chemically induced/*drug therapy/pathology
MH  - Cyclooxygenase 2/metabolism
MH  - Dextran Sulfate/toxicity
MH  - Disease Models, Animal
MH  - Female
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Peroxidase/antagonists & inhibitors
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors
EDAT- 2006/10/04 09:00
MHDA- 2007/01/11 09:00
CRDT- 2006/10/04 09:00
PHST- 2006/10/04 09:00 [pubmed]
PHST- 2007/01/11 09:00 [medline]
PHST- 2006/10/04 09:00 [entrez]
PST - ppublish
SO  - Int J Mol Med. 2006 Nov;18(5):893-9.