Abstract：
OBJECTIVES:Inflammation may directly impair HDL functions, in particular reverse cholesterol transport (RCT), but limited data support this concept in humans. METHODS AND RESULTS:We employed low-dose human endotoxemia to assess the effects of inflammation on HDL and RCT-related parameters in vivo. Endotoxemia induced remodelling of HDL with depletion of pre-β1a HDL particles determined by 2-D gel electrophoresis (-32.2±9.3% at 24 h, p<0.05) as well as small (-23.0±5.1%, p<0.01, at 24 h) and medium (-57.6±8.0% at 16 h, p<0.001) HDL estimated by nuclear magnetic resonance (NMR). This was associated with induction of class II secretory phospholipase A2 (~36 fold increase) and suppression of lecithin:cholesterol acyltransferase activity (-20.8±3.4% at 24 h, p<0.01) and cholesterol ester transfer protein mass (-22.2±6.8% at 24 h, p<0.001). The HDL fraction, isolated following endotoxemia, had reduced capacity to efflux cholesterol in vitro from SR-BI and ABCA1, but not ABCG1 transporter cell models. CONCLUSIONS:These data support the concept that "atherogenic-HDL dysfunction" and impaired RCT occur in human inflammatory syndromes, largely independent of changes in plasma HDL-C and ApoA-I levels.
journal_name
Atherosclerosisjournal_title
Atherosclerosisauthors
de la Llera Moya M,McGillicuddy FC,Hinkle CC,Byrne M,Joshi MR,Nguyen V,Tabita-Martinez J,Wolfe ML,Badellino K,Pruscino L,Mehta NN,Asztalos BF,Reilly MPdoi
10.1016/j.atherosclerosis.2012.02.032subject
Has Abstractpub_date
2012-06-01 00:00:00pages
390-4issue
2eissn
0021-9150issn
1879-1484pii
S0021-9150(12)00146-3journal_volume
222pub_type
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