PMID- 11290601
OWN - NLM
STAT- MEDLINE
DCOM- 20010524
LR  - 20210216
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 97
IP  - 8
DP  - 2001 Apr 15
TI  - Apolipoprotein A-I inhibits the production of interleukin-1beta and tumor 
      necrosis factor-alpha by blocking contact-mediated activation of monocytes by T 
      lymphocytes.
PG  - 2381-9
AB  - Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta), 
      essential components in the pathogenesis of immunoinflammatory diseases, are 
      strongly induced in monocytes by direct contact with stimulated T lymphocytes. 
      This study demonstrates that adult human serum (HS) but not fetal calf or cord 
      blood serum displays inhibitory activity toward the contact-mediated activation 
      of monocytes by stimulated T cells, decreasing the production of both TNF-alpha 
      and IL-1beta. Fractionation of HS and N-terminal microsequencing as well as 
      electroelution of material subjected to preparative electrophoresis revealed that 
      apolipoprotein A-I (apo A-I), a "negative" acute-phase protein, was the 
      inhibitory factor. Functional assays and flow cytometry analyses show that 
      high-density lipoprotein (HDL)-associated apo A-I inhibits contact-mediated 
      activation of monocytes by binding to stimulated T cells, thus inhibiting 
      TNF-alpha and IL-1beta production at both protein and messenger RNA levels. 
      Furthermore, apo A-I inhibits monocyte inflammatory functions in peripheral blood 
      mononuclear cells activated by either specific antigens or lectins without 
      affecting cell proliferation. These results demonstrate a new anti-inflammatory 
      activity of HDL-associated apo A-I that might have modulating functions in 
      nonseptic conditions. Therefore, because HDL has been shown to bind and 
      neutralize lipopolysaccharide, HDL appears to play an important part in 
      modulating both acute and chronic inflammation. The novel anti-inflammatory 
      function of apo A-I reported here might lead to new therapeutic approaches in 
      inflammatory diseases such as rheumatoid arthritis, multiple sclerosis, systemic 
      lupus erythematosus, and atherosclerosis.
FAU - Hyka, N
AU  - Hyka N
AD  - Division of Immunology and Allergy (Hans Wilsdorf Laboratory), Department of 
      Internal Medicine, University Hospital, Geneve, Switzerland.
FAU - Dayer, J M
AU  - Dayer JM
FAU - Modoux, C
AU  - Modoux C
FAU - Kohno, T
AU  - Kohno T
FAU - Edwards, C K 3rd
AU  - Edwards CK 3rd
FAU - Roux-Lombard, P
AU  - Roux-Lombard P
FAU - Burger, D
AU  - Burger D
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (Apolipoprotein A-I)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Lipoproteins, HDL)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Acute-Phase Reaction
MH  - Adult
MH  - Animals
MH  - Apolipoprotein A-I/isolation & purification/*pharmacology
MH  - Cattle
MH  - Cell Communication/*drug effects
MH  - Depression, Chemical
MH  - Drug Design
MH  - Fetal Blood
MH  - Gene Expression Regulation/drug effects
MH  - Humans
MH  - Infant, Newborn
MH  - Inflammation
MH  - Interleukin-1/*biosynthesis/genetics
MH  - Lipopolysaccharides/antagonists & inhibitors/pharmacology
MH  - Lipoproteins, HDL/isolation & purification/*physiology
MH  - Mice
MH  - Monocytes/*drug effects/metabolism
MH  - RNA, Messenger/biosynthesis
MH  - T-Lymphocytes/*physiology
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/*biosynthesis/genetics
EDAT- 2001/04/06 10:00
MHDA- 2001/05/26 10:01
CRDT- 2001/04/06 10:00
PHST- 2001/04/06 10:00 [pubmed]
PHST- 2001/05/26 10:01 [medline]
PHST- 2001/04/06 10:00 [entrez]
AID - S0006-4971(20)55761-3 [pii]
AID - 10.1182/blood.v97.8.2381 [doi]
PST - ppublish
SO  - Blood. 2001 Apr 15;97(8):2381-9. doi: 10.1182/blood.v97.8.2381.