PMID- 15777559
OWN - NLM
STAT- MEDLINE
DCOM- 20050628
LR  - 20220317
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 179
IP  - 2
DP  - 2005 Apr
TI  - Folic acid reverses hyper-responsiveness of LPS-induced chemokine secretion from 
      monocytes in patients with hyperhomocysteinemia.
PG  - 395-402
AB  - Our previous study demonstrated that homocysteine (Hcy) mediated the expression 
      and secretion of MCP-1 and IL-8 in human monocytes. In the present study, we 
      investigated whether the responsiveness of isolated monocytes to 
      lipopolysaccharide (LPS)-induced chemokine secretion was enhanced in patients 
      with hyperhomocysteinemia (HHcy), and if so, whether this enhanced response could 
      be inhibited by folic acid treatment. We studied 38 control subjects and 40 
      patients with HHcy. The results showed that MCP-1 secretion from isolated 
      monocytes in response to low-dose LPS in patients with HHcy was significantly 
      higher than that in controls. After patients with HHcy underwent low-dose folic 
      acid treatment (0.8 mg/d) for 6 months, plasma Hcy levels were decreased and the 
      hyper-responsiveness of MCP-1 and IL-8 secreted by isolated monocytes was 
      significantly reversed. Furthermore, folic acid treatment at high concentrations 
      (5 microM) significantly reduced the elevated levels of reactive oxygen species, 
      NADPH oxidase activity and chemokines in response to Hcy in cultured human 
      monocytes. HHcy may contribute to atherogenesis through enhancing the 
      responsiveness of monocytes to inflammatory stimuli and promoting leukocyte 
      recruitment into atherosclerotic plaque. In addition to lowering the plasma 
      levels of Hcy, low-dose folic acid treatment exerts beneficial effects on 
      patients with HHcy by inhibiting pro-inflammatory responses such as chemokine 
      secretion from human monocytes.
FAU - Wang, Guang
AU  - Wang G
AD  - Institute of Vascular Medicine, Peking University Third Hospital, Beijing 100083, 
      PR China.
FAU - Dai, Jing
AU  - Dai J
FAU - Mao, Jieming
AU  - Mao J
FAU - Zeng, Xiaokun
AU  - Zeng X
FAU - Yang, Xiaoda
AU  - Yang X
FAU - Wang, Xian
AU  - Wang X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20050101
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Chemokines)
RN  - 0 (Hematinics)
RN  - 0 (Lipopolysaccharides)
RN  - 935E97BOY8 (Folic Acid)
RN  - EC 1.6.3.- (NADPH Oxidases)
SB  - IM
MH  - Arteriosclerosis/*drug therapy/immunology
MH  - Case-Control Studies
MH  - Cell Culture Techniques
MH  - Chemokines/*metabolism
MH  - Folic Acid/*pharmacology
MH  - Hematinics/*pharmacology
MH  - Humans
MH  - Hyperhomocysteinemia
MH  - Inflammation
MH  - Lipopolysaccharides/*pharmacology
MH  - Monocytes/*physiology
MH  - NADPH Oxidases/pharmacology
EDAT- 2005/03/22 09:00
MHDA- 2005/06/29 09:00
CRDT- 2005/03/22 09:00
PHST- 2004/01/22 00:00 [received]
PHST- 2004/07/21 00:00 [revised]
PHST- 2004/10/25 00:00 [accepted]
PHST- 2005/03/22 09:00 [pubmed]
PHST- 2005/06/29 09:00 [medline]
PHST- 2005/03/22 09:00 [entrez]
AID - S0021-9150(04)00570-2 [pii]
AID - 10.1016/j.atherosclerosis.2004.10.033 [doi]
PST - ppublish
SO  - Atherosclerosis. 2005 Apr;179(2):395-402. doi: 
      10.1016/j.atherosclerosis.2004.10.033. Epub 2005 Jan 1.