PMID- 19214726
OWN - NLM
STAT- MEDLINE
DCOM- 20090617
LR  - 20211020
IS  - 1573-2576 (Electronic)
IS  - 0360-3997 (Linking)
VI  - 32
IP  - 2
DP  - 2009 Apr
TI  - Inhalation of carbon monoxide ameliorates collagen-induced arthritis in mice and 
      regulates the articular expression of IL-1beta and MCP-1.
PG  - 83-8
LID - 10.1007/s10753-009-9106-6 [doi]
AB  - Carbon monoxide (CO), long considered a toxic gas, has recently been shown to 
      mediate anti-inflammatory effects in various animal models. The aim of this study 
      was to investigate whether the inhalation of CO ameliorated collagen-induced 
      arthritis (CIA) in mice. CIA was induced in female DBA/1 mice by the injection of 
      an anti-type II collagen antibody and lipopolysaccharide. The CO treatment group 
      was exposed to CO gas at a concentration of 200 ppm in a closed cage starting on 
      the day of the injection with an anti-type II collagen antibody and throughout 
      the remaining study period. The clinical arthritis scores was examined daily for 
      swelling of the paws as a sign of arthritis. For histopathology, the sections of 
      the hind legs were evaluated by hematoxylin-eosin staining. Moreover, we 
      evaluated the expression of interleukin (IL)-1beta and monocyte chemoattractant 
      protein-1 (MCP-1) mRNA in the hind paws. Both clinical arthritis scores as well 
      as histological findings of joint inflammation were significantly reduced in mice 
      treated with CO gas inhalation compared to untreated mice. Further, CO 
      significantly inhibited the increased expression of IL-1beta and MCP-1 mRNA in 
      paws at day 3 after the induction of arthritis. In conclusion, the inhalation of 
      CO protected mice from the synovial inflammation of CIA. Based on these data, the 
      beneficial effects of CO in murine RA model may be attributed to its 
      anti-inflammatory properties.
FAU - Takagi, Tomohisa
AU  - Takagi T
AD  - Department of Molecular Gastroenterology and Hepatology, Graduate School of 
      Medical Sience, Kyoto Prefectural University of Medicine, 465 Kajii-cho, 
      Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
FAU - Naito, Yuji
AU  - Naito Y
FAU - Inoue, Mamoru
AU  - Inoue M
FAU - Akagiri, Satomi
AU  - Akagiri S
FAU - Mizushima, Katsura
AU  - Mizushima K
FAU - Handa, Osamu
AU  - Handa O
FAU - Kokura, Satoshi
AU  - Kokura S
FAU - Ichikawa, Hiroshi
AU  - Ichikawa H
FAU - Yoshikawa, Toshikazu
AU  - Yoshikawa T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Inflammation
JT  - Inflammation
JID - 7600105
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-1beta)
RN  - 0 (RNA, Messenger)
RN  - 7U1EE4V452 (Carbon Monoxide)
RN  - 9007-34-5 (Collagen)
SB  - IM
MH  - Animals
MH  - Arthritis, Experimental/*therapy
MH  - Carbon Monoxide/*administration & dosage/therapeutic use
MH  - Cartilage, Articular/*metabolism
MH  - Chemokine CCL2/*genetics
MH  - Collagen/adverse effects
MH  - Female
MH  - Gene Expression Regulation/*drug effects
MH  - Inflammation/prevention & control
MH  - Interleukin-1beta/*genetics
MH  - Mice
MH  - Mice, Inbred Strains
MH  - RNA, Messenger/analysis
MH  - Severity of Illness Index
EDAT- 2009/02/14 09:00
MHDA- 2009/06/18 09:00
CRDT- 2009/02/14 09:00
PHST- 2009/02/14 09:00 [entrez]
PHST- 2009/02/14 09:00 [pubmed]
PHST- 2009/06/18 09:00 [medline]
AID - 10.1007/s10753-009-9106-6 [doi]
PST - ppublish
SO  - Inflammation. 2009 Apr;32(2):83-8. doi: 10.1007/s10753-009-9106-6.