PMID- 21163482
OWN - NLM
STAT- MEDLINE
DCOM- 20110523
LR  - 20190816
IS  - 1879-1484 (Electronic)
IS  - 0021-9150 (Linking)
VI  - 214
IP  - 2
DP  - 2011 Feb
TI  - OxLDL-IgG immune complexes induce expression and secretion of proatherogenic 
      cytokines by cultured human mast cells.
PG  - 357-63
LID - 10.1016/j.atherosclerosis.2010.11.024 [doi]
AB  - OBJECTIVE: Human atherosclerotic lesions contain mast cells and immunoglobulin G 
      immune complexes containing oxidized low-density lipoproteins (oxLDL-IgG ICs). 
      Here we studied whether such oxLDL-IgG ICs can activate human mast cells and 
      induce them to express and secrete pro-inflammatory cytokines that are 
      potentially capable of inducing and amplifying atherogenic processes. METHODS AND 
      RESULTS: Incubation of cultured human mast cells in the presence of oxLDL-IgG ICs 
      led to a significant dose-dependent upregulation of the expression and secretion 
      of tumor necrosis factor-alpha (TNF-a) and interleukin-8 (IL-8), and the 
      chemotactic cytokine monocyte chemoattractant protein-1 (MCP-1). The secretory 
      responses were dose-dependent and associated with moderate release of histamine 
      and tryptase, which are preformed mast cell mediators contained in the 
      cytoplasmic secretory granules of the cells. Also native LDL-IgG ICs induced 
      similar pro-inflammatory cytokine response, suggesting that ICs per se are 
      important for the IgG IC-induced mast cell activation. CONCLUSION: Mast cells in 
      atherosclerotic lesions which also contain oxLDL-IgG ICs may become activated by 
      the ICs and secrete many pro-inflammatory cytokines. Our results suggest that 
      intimal mast cells act as a cellular link between oxLDL-IgG ICs and the 
      inflammatory response in atherosclerosis.
CI  - Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.
FAU - Lappalainen, Jani
AU  - Lappalainen J
AD  - Wihuri Research Institute, Kalliolinnantie 4, FI-00140 Helsinki, Finland. 
      jani.lappalainen@helsinki.fi
FAU - Lindstedt, Ken A
AU  - Lindstedt KA
FAU - Oksjoki, Riina
AU  - Oksjoki R
FAU - Kovanen, Petri T
AU  - Kovanen PT
LA  - eng
PT  - Journal Article
DEP - 20101126
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Antigen-Antibody Complex)
RN  - 0 (CCL2 protein, human)
RN  - 0 (CXCL8 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (oxidized low density lipoprotein)
RN  - EC 3.4.21.59 (Tryptases)
SB  - IM
MH  - Antigen-Antibody Complex/*metabolism
MH  - Atherosclerosis/*immunology
MH  - Cells, Cultured
MH  - Chemokine CCL2/metabolism
MH  - Cytokines/genetics/*metabolism
MH  - Gene Expression Regulation
MH  - Histamine Release
MH  - Humans
MH  - Immunoglobulin G/*metabolism
MH  - Inflammation Mediators/*metabolism
MH  - Interleukin-8/metabolism
MH  - Lipoproteins, LDL/*immunology
MH  - Mast Cells/*immunology
MH  - RNA, Messenger/metabolism
MH  - Signal Transduction
MH  - Time Factors
MH  - Tryptases/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2010/12/18 06:00
MHDA- 2011/05/24 06:00
CRDT- 2010/12/18 06:00
PHST- 2010/08/12 00:00 [received]
PHST- 2010/11/19 00:00 [revised]
PHST- 2010/11/19 00:00 [accepted]
PHST- 2010/12/18 06:00 [entrez]
PHST- 2010/12/18 06:00 [pubmed]
PHST- 2011/05/24 06:00 [medline]
AID - S0021-9150(10)00963-9 [pii]
AID - 10.1016/j.atherosclerosis.2010.11.024 [doi]
PST - ppublish
SO  - Atherosclerosis. 2011 Feb;214(2):357-63. doi: 
      10.1016/j.atherosclerosis.2010.11.024. Epub 2010 Nov 26.