PMID- 18242212
OWN - NLM
STAT- MEDLINE
DCOM- 20080214
LR  - 20220317
IS  - 1528-0012 (Electronic)
IS  - 0016-5085 (Linking)
VI  - 134
IP  - 2
DP  - 2008 Feb
TI  - A critical role of CD30 ligand/CD30 in controlling inflammatory bowel diseases in 
      mice.
PG  - 447-58
LID - 10.1053/j.gastro.2007.11.004 [doi]
AB  - BACKGROUND & AIMS: A CD30-ligand (CD30L) is a 40-kilodalton, type II 
      membrane-associated glycoprotein belonging to the tumor necrosis factor family. 
      Serum levels of soluble CD30 increased in inflammatory bowel diseases (IBD), 
      suggesting that CD30L/CD30 signaling is involved in the pathogenesis of IBD. In 
      this study, we investigated the role of CD30L in oxazolone (OXA)- and 
      trinitrobenzene sulfonic acid (TNBS)-induced colitis in CD30L knockout (KO) mice. 
      METHODS: Colitis was induced by OXA or TNBS in CD30LKO mice with BALB/c or 
      C57BL/6 background, respectively, and diverse clinical signs of the disease were 
      evaluated. Cytokine production from lamina propria T cells of the colon was 
      assessed by enzyme-linked immunosorbent assay. Anti-interleukin (IL)-4 monoclonal 
      antibody (mAb) or agonistic anti-CD30 mAb was inoculated in mice with colitis 
      induced by OXA or TNBS. RESULTS: CD30LKO mice were susceptible to OXA-induced 
      colitis but resistant to TNBS-induced acute colitis. The levels of T helper cell 
      2 type cytokines such as IL-4 and IL-13 in the LP T cells were significantly 
      higher, but the levels of interferon gamma were lower in OXA- or TNBS-treated 
      CD30LKO mice than in wild-type mice. In vivo administration of agonistic 
      anti-CD30 mAb ameliorated OXA-induced colitis but aggravated TNBS-induced colitis 
      in CD30LKO mice. CONCLUSIONS: These results suggest that CD30L/CD30 signaling is 
      involved in development of both OXA- and TNBS-induced colitis. Modulation of 
      CD30L/CD30 signaling by mAb could be a novel biologic therapy for IBD.
FAU - Sun, Xun
AU  - Sun X
AD  - Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, 
      Fukuoka, Japan.
FAU - Somada, Shinichi
AU  - Somada S
FAU - Shibata, Kensuke
AU  - Shibata K
FAU - Muta, Hiromi
AU  - Muta H
FAU - Yamada, Hisakata
AU  - Yamada H
FAU - Yoshihara, Hirofumi
AU  - Yoshihara H
FAU - Honda, Kuniomi
AU  - Honda K
FAU - Nakamura, Kazuhiko
AU  - Nakamura K
FAU - Takayanagi, Ryhoichi
AU  - Takayanagi R
FAU - Tani, Kenzaburo
AU  - Tani K
FAU - Podack, Eckhard R
AU  - Podack ER
FAU - Yoshikai, Yasunobu
AU  - Yoshikai Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20071104
PL  - United States
TA  - Gastroenterology
JT  - Gastroenterology
JID - 0374630
RN  - 0 (Adjuvants, Immunologic)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (CD30 Ligand)
RN  - 0 (Cytokines)
RN  - 0 (Ki-1 Antigen)
RN  - 15646-46-5 (Oxazolone)
RN  - 207137-56-2 (Interleukin-4)
RN  - 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid)
SB  - IM
MH  - Adjuvants, Immunologic
MH  - Animals
MH  - Antibodies, Monoclonal/immunology/therapeutic use
MH  - CD30 Ligand/genetics/*physiology
MH  - Colitis/chemically induced/genetics/*physiopathology
MH  - Cytokines/metabolism
MH  - Disease Models, Animal
MH  - Genetic Predisposition to Disease
MH  - Inflammatory Bowel Diseases/chemically induced/genetics/*physiopathology
MH  - Interleukin-4/immunology
MH  - Intestinal Mucosa/metabolism/pathology
MH  - Ki-1 Antigen/genetics/immunology/*physiology
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Oxazolone
MH  - Signal Transduction/physiology
MH  - Trinitrobenzenesulfonic Acid
EDAT- 2008/02/05 09:00
MHDA- 2008/02/15 09:00
CRDT- 2008/02/05 09:00
PHST- 2007/04/29 00:00 [received]
PHST- 2007/10/25 00:00 [accepted]
PHST- 2008/02/05 09:00 [pubmed]
PHST- 2008/02/15 09:00 [medline]
PHST- 2008/02/05 09:00 [entrez]
AID - S0016-5085(07)01994-4 [pii]
AID - 10.1053/j.gastro.2007.11.004 [doi]
PST - ppublish
SO  - Gastroenterology. 2008 Feb;134(2):447-58. doi: 10.1053/j.gastro.2007.11.004. Epub 
      2007 Nov 4.