PMID- 19890701
OWN - NLM
STAT- MEDLINE
DCOM- 20100903
LR  - 20211020
IS  - 1573-2592 (Electronic)
IS  - 0271-9142 (Linking)
VI  - 30
IP  - 2
DP  - 2010 Mar
TI  - The vagus nerve and nicotinic receptors involve inhibition of HMGB1 release and 
      early pro-inflammatory cytokines function in collagen-induced arthritis.
PG  - 213-20
LID - 10.1007/s10875-009-9346-0 [doi]
AB  - OBJECTIVES: The cholinergic anti-inflammatory pathway, a vagus nerve-dependent 
      mechanism, inhibits cytokine releases in models of acute inflammatory disease. We 
      investigated the efficacy and elucidated the possible mechanism of the 
      cholinergic anti-inflammatory pathway on collagen-induced arthritis (CIA) in 
      mice. METHODS: Fifty-six male DBA/1 mice were divided into four groups: control 
      mice (sham vagotomy + phosphate-buffered saline; shamVGX+PBS), model mice 
      (shamVGX+PBS+CIA), vagotomy mice (VGX+PBS+CIA), and nicotine (Nic) mice 
      (shamVGX+Nic+CIA). We subjected mice to left-side cervical vagotomy 4 days before 
      induction of arthritis. Mice in the nicotine group were injected with nicotine 
      (250 microg/kg per day) 4 days before arthritis induction. Arthritis score was 
      measured and histopathologic assessment of joint sections carried out. The 
      concentration of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-10 
      in serum were evaluated by ELISA. Expression of high-mobility group box 
      chromosomal protein 1(HMGB1) was evaluated by immunohistochemical staining of 
      joints. RESULTS: Vagotomy exaggerated, whereas nicotine attenuated, clinical 
      arthritis. Histopathologic findings confirmed that nicotine reduced infiltration 
      of inflammatory cell and bone destruction. Expression of TNF-alpha and IL-6 
      decreased in nicotine-pretreated mice compared with model and vagotomy mice; 
      IL-10 levels were not significantly different between the model group and 
      nicotine group. Nicotine reduced the expression and translocation of HMGB1 in the 
      inflamed joints of CIA mice. CONCLUSIONS: The cholinergic anti-inflammatory 
      pathway has an anti-inflammatory role in the pathophysiology of rheumatoid 
      arthritis (RA) via inhibiting HMGB1 release and early pro-inflammatory cytokines 
      function. Study of this pathway could be used for RA therapy.
FAU - Li, Tong
AU  - Li T
AD  - Department of Rheumatology, Xiangya Hospital, Central South University, Changsha, 
      Hunan, People's Republic of China.
FAU - Zuo, Xiaoxia
AU  - Zuo X
FAU - Zhou, Yaou
AU  - Zhou Y
FAU - Wang, Yanping
AU  - Wang Y
FAU - Zhuang, Hanping
AU  - Zhuang H
FAU - Zhang, Lingli
AU  - Zhang L
FAU - Zhang, Huali
AU  - Zhang H
FAU - Xiao, Xianzhong
AU  - Xiao X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20091105
PL  - Netherlands
TA  - J Clin Immunol
JT  - Journal of clinical immunology
JID - 8102137
RN  - 0 (Cholinergic Agents)
RN  - 0 (Collagen Type II)
RN  - 0 (Cytokines)
RN  - 0 (HMGB1 Protein)
RN  - 0 (Receptors, Nicotinic)
RN  - 6M3C89ZY6R (Nicotine)
SB  - IM
MH  - Animals
MH  - Arthritis, Experimental/blood/chemically induced/*immunology/physiopathology
MH  - Cattle
MH  - Cholinergic Agents/administration & dosage
MH  - Collagen Type II/administration & dosage
MH  - Cytokines/antagonists & inhibitors/blood
MH  - Disease Progression
MH  - HMGB1 Protein/*antagonists & inhibitors
MH  - Inflammation
MH  - Male
MH  - Mice
MH  - Mice, Inbred DBA
MH  - Nicotine/*administration & dosage
MH  - Receptors, Nicotinic/*metabolism
MH  - Synovial Membrane/pathology
MH  - Vagotomy
MH  - Vagus Nerve/drug effects/*immunology/surgery
EDAT- 2009/11/06 06:00
MHDA- 2010/09/04 06:00
CRDT- 2009/11/06 06:00
PHST- 2009/09/05 00:00 [received]
PHST- 2009/10/22 00:00 [accepted]
PHST- 2009/11/06 06:00 [entrez]
PHST- 2009/11/06 06:00 [pubmed]
PHST- 2010/09/04 06:00 [medline]
AID - 10.1007/s10875-009-9346-0 [doi]
PST - ppublish
SO  - J Clin Immunol. 2010 Mar;30(2):213-20. doi: 10.1007/s10875-009-9346-0. Epub 2009 
      Nov 5.