Chiara Pavanello, Italy
Università degli Studi di Milano Dipartimento di Scienze Farmacologiche e Biomolecolari
Presenter of 2 Presentations
Live Q&A
Session Time
13:00 - 14:00
Lecture Time
13:30 - 14:00
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[session]
[presentation]
[presenter]
Effects of APOA1, ABCA1 and LCAT Mutations on Monocyte Activation in Humans – a Double Edged Sword
Session Time
13:00 - 14:00
Lecture Time
13:20 - 13:25
Background and Aims
Plasma high-density lipoprotein cholesterol (HDL-C) levels are inversely associated with cardiovascular disease risk. Whereas the causal nature of this relationship was challenged by genetic studies and several outcome trials, an increasing number of animal and in vitro studies emphasized the effects of HDL on the immune system. In vivo data supporting these effects on monocytes in patients are lacking. Here, we evaluated whether low levels of HDL-C determined by genetic mutations (e.g. ABCA1, APOA1 and LCAT) are associated with monocyte activation in humans.
Methods
We compared the monocyte phenotype from subjects with low-HDL (either ABCA1, apoA-I or LCAT deficient) to normolipidemic healthy controls. We used flow cytometry, measured intracellular lipid content as well as used functional read-outs such as trans-endothelial migration capacity and cytokine production. Finally, we studied RNA expression of pivotal inflammatory as well as cholesterol homeostasis genes.
Results
We found that apoA-I and ABCA1 deficiency associate with a pro-inflammatory monocyte phenotype with increased levels of activation markers, increased cytokine production and transendothelial migration capacity compared to controls. Baseline expression of IL-1b was increased. In contrast, LCAT deficiency shows an opposite phenotype with reduced transendothelial migration capacity and increased expression of efflux receptors. This is accompanied by a decreased cytokine production capacity and lower activation markers.
Conclusions
Different HDL-genotypes are associated with lead opposite monocyte immunophenotypes, resulting in either pro- or anti-inflammatory monocytes. Monocytes from HDL-deficient patients have a genotype specific pro- or anti-inflammatory phenotype and HDL-deficient patients may therefore benefit from optimization of a more personalized treatment strategy.
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