PMID- 16412693
OWN - NLM
STAT- MEDLINE
DCOM- 20060623
LR  - 20131121
IS  - 1521-6616 (Print)
IS  - 1521-6616 (Linking)
VI  - 119
IP  - 3
DP  - 2006 Jun
TI  - Anti-inflammatory effect of all-trans-retinoic acid in inflammatory arthritis.
PG  - 272-9
AB  - OBJECTIVE: To determine whether all-trans-retinoic acid (ATRA) improves the 
      destruction of joints and the effect of cytokines on DBA/1J mice with 
      collagen-induced arthritis (CIA). METHODS: Starting from the time of type II 
      collagen injection, DBA/1J mice were injected intraperitoneally with PBS or 0.5 
      mg of ATRA 3 times per week for 35 days. The effects of treatment were monitored 
      by determining arthritis and histological scores and measuring cellular 
      proliferation, production of cytokines (IL-2, IL-10, IL-12, IL-6, IFN-gamma, and 
      TNF-alpha) and IgG, and the expression of mRNAs for inducible nitric oxide 
      synthase (iNOS), monocyte chemoattractant protein-1 (MCP-1), and CXCR3. RESULTS: 
      The arthritis score and incidence of arthritis were lower in the mice treated 
      with ATRA than in those treated with PBS. Histopathologic evidence of joint 
      damage was 34% lower, and the infiltrations of macrophages were reduced in the 
      mice treated with ATRA compared with those treated with PBS. Type II collagen- 
      and ConA-stimulated proliferation of spleen cells, the production of cytokines 
      (IL-6, IL-12, and TNF-alpha), the serum levels of total IgG and IgG1 
      anti-collagen antibodies, and the expression of mRNAs for MCP-1 were 
      significantly reduced in the mice treated with ATRA than in those treated with 
      PBS. CONCLUSION: ATRA improved the clinical course and reduced the production of 
      inflammatory cytokines, immunoglobulin, and chemokines in murine CIA. These data 
      suggest that ATRA might be also effective for the treatment of inflammatory 
      arthritis like human rheumatoid arthritis.
FAU - Nozaki, Yuji
AU  - Nozaki Y
AD  - Department of Nephrology and Rheumatology, Kinki University School of Medicine, 
      377-2 Ohno-Higashi, Osaka-Sayama, Osaka, 589-8511, Japan.
FAU - Yamagata, Toshiaki
AU  - Yamagata T
FAU - Sugiyama, Masafumi
AU  - Sugiyama M
FAU - Ikoma, Shinya
AU  - Ikoma S
FAU - Kinoshita, Koji
AU  - Kinoshita K
FAU - Funauchi, Masanori
AU  - Funauchi M
LA  - eng
PT  - Journal Article
DEP - 20060110
PL  - United States
TA  - Clin Immunol
JT  - Clinical immunology (Orlando, Fla.)
JID - 100883537
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (CXCR3 protein, human)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cxcr3 protein, mouse)
RN  - 0 (Cytokines)
RN  - 0 (Immunoglobulin G)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, CXCR3)
RN  - 0 (Receptors, Chemokine)
RN  - 5688UTC01R (Tretinoin)
RN  - 9007-34-5 (Collagen)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.13.39 (Nos2 protein, mouse)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/therapeutic use
MH  - Arthritis, Experimental/chemically induced/*drug therapy/prevention & control
MH  - Cell Proliferation
MH  - Chemokine CCL2/genetics/metabolism
MH  - Collagen/immunology/pharmacology
MH  - Cytokines/immunology
MH  - Gene Expression Regulation
MH  - Immunoglobulin G/blood
MH  - Joints/drug effects/pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred DBA
MH  - Nitric Oxide Synthase Type II/genetics/metabolism
MH  - RNA, Messenger/metabolism
MH  - Receptors, CXCR3
MH  - Receptors, Chemokine/genetics/metabolism
MH  - Spleen/drug effects/immunology/metabolism
MH  - Tretinoin/*therapeutic use
EDAT- 2006/01/18 09:00
MHDA- 2006/06/24 09:00
CRDT- 2006/01/18 09:00
PHST- 2005/10/21 00:00 [received]
PHST- 2005/11/26 00:00 [revised]
PHST- 2005/11/28 00:00 [accepted]
PHST- 2006/01/18 09:00 [pubmed]
PHST- 2006/06/24 09:00 [medline]
PHST- 2006/01/18 09:00 [entrez]
AID - S1521-6616(05)00390-6 [pii]
AID - 10.1016/j.clim.2005.11.012 [doi]
PST - ppublish
SO  - Clin Immunol. 2006 Jun;119(3):272-9. doi: 10.1016/j.clim.2005.11.012. Epub 2006 
      Jan 10.