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    HDL in infectious diseases and sepsis

    Access Status
    Fulltext not available
    Authors
    Pirillo, A.
    Catapano, A.
    Norata, Giuseppe
    Date
    2015
    Type
    Conference Paper
    
    Metadata
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    Citation
    Pirillo, A. and Catapano, A. and Norata, G. 2015. HDL in infectious diseases and sepsis, pp. 483-508.
    Source Title
    Handbook of Experimental Pharmacology
    DOI
    10.1007/978-3-319-09665-0_15
    ISSN
    0171-2004
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/55147
    Collection
    • Curtin Research Publications
    Abstract

    © The Author(s) 2015. During infection significant alterations in lipid metabolism and lipoprotein composition occur. Triglyceride and VLDL cholesterol levels increase, while reduced HDL cholesterol (HDL-C) and LDL cholesterol (LDL-C) levels are observed. More importantly, endotoxemia modulates HDL composition and size: phospholipids are reduced as well as apolipoprotein (apo) A-I, whileserum amyloid A (SAA) and secretory phospholipase A2 (sPLA2) dramatically increase, and, although the total HDL particle number does not change, a significant decrease in the number of small- and medium-size particles is observed. Low HDL-C levels inversely correlate with the severity of septic disease and associate with an exaggerated systemic inflammatory response. HDL, as well as other plasma lipoproteins, can bind and neutralize Gramnegative bacterial lipopolysaccharide (LPS) and Gram-positive bacterial lipoteichoic acid (LTA), thus favoring the clearance of these products. HDLs are emerging also as a relevant player during parasitic infections, and a specific component of HDL, namely, apoL-1, confers innate immunity against trypanosome by favoring lysosomal swelling which kills the parasite. During virus infections, proteins associated with the modulation of cholesterol bioavailability in the lipid rafts such as ABCA1 and SR-BI have been shown to favor virus entry into the cells. Pharmacological studies support the benefit of recombinant HDL or apoA-I mimetics during bacterial infection, while apoL-1-nanobody complexes were tested for trypanosome infection. Finally, SR-BI antagonism represents a novel and forefront approach interfering with hepatitis C virus entry which is currently tested in clinical studies. From the coming years, we have to expect new and compelling observations further linking HDL to innate immunity and infections.

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