Effects of human apolipoprotein A-I on endotoxin-induced leukocyte adhesion on endothelial cells in vivo and on the growth of Escherichia coli in vitro

Thaveeratitham, Premtip; Plengpanich, Wanee; Naen-Udorn, Worakamol; Patumraj, Suthiluk; Khovidhunkit, Weerapan

doi:10.1177/0968051907078611

Cited by 19 publications

(15 citation statements)

References 32 publications

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“…Studies conducted in Oncorhynchus mykiss (Rainbow trout) have confirmed the expression of apoA-I in some of the most important epithelial and mucosal layers [13]. HDL and apoA-I have also been demonstrated to have antimicrobial properties [12,194] inhibiting the growth of Escherichia coli and Staphylococcus epidermidis [173,195], a finding largely attributable to apoA-I. Another innate immune related role of apoA-I which was also discovered in fish is its regulation of the complement system [11].…”

Section: Other Roles In the Innate Immune Response Antiviral Andmentioning

confidence: 82%

“…In vivo studies conducted in mice and rats have demonstrated that both HDL and apoA-I can reduce leukocyte adhesion and protect against the inflammatory effects of LPS, largely thought to be mediated via the protein component of HDL (i.e., apoA-I) [172][173][174]. A study by Thaveeratitham et al demonstrated that rHDL dose dependently decreases monocyte activation to LPS; however, this was not seen by mature HDL, giving further evidence that apoA-I may be the major protective molecule [173,175].…”

Section: Leukocytesmentioning

confidence: 99%

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High Density Lipoprotein: Assembly, Structure, Cargo, and Functions

Murphy

2013

ISRN Physiology

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Cardiovascular disease (CVD) is the leading cause of death globally. For close to four decades, we have known that high density lipoprotein (HDL) levels are inversely correlated with the risk of CVD. HDL is a complex particle that consists of proteins, phospholipids, and cholesterol and has the ability to carry micro-RNAs. HDL is constantly undergoing remodelling throughout its life-span and carries out many functions. This review summarizes many of the different aspects of HDL from its assembly, the receptors it interacts with, along with the functions it performs and how it can be altered in disease. While HDL is a key cholesterol efflux particle, this review highlights the many other important functions of HDL in the innate immune system and details the potential therapeutic uses of HDL outside of CVD.

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Section: Other Roles In the Innate Immune Response Antiviral Andmentioning

confidence: 82%

Section: Leukocytesmentioning

confidence: 99%

High Density Lipoprotein: Assembly, Structure, Cargo, and Functions

Murphy

2013

ISRN Physiology

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“…Recently Samanovic et al (4) reported that TLF effectively kills Leishmania promastigotes within the parasitophorous vacuole of macrophages. Additionally, it is known that apoA-1 binds the bacterial outer membrane component lipopolysaccharide (38 -40), protects against the toxic effects of this molecule in vivo (41), and inhibits the growth of Escherichia coli in vitro (42). Thus it is intriguing to consider the possibility that the membrane-destabilizing activity of TLF is also an effective mechanism of combating bacterial infection.…”

Section: Discussionmentioning

confidence: 99%

Membrane Permeabilization by Trypanosome Lytic Factor, a Cytolytic Human High Density Lipoprotein

Harrington

Howell

Hajduk

2009

Journal of Biological Chemistry

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Trypanosome lytic factor (TLF) is a subclass of human high density lipoprotein (HDL) that mediates an innate immune killing of certain mammalian trypanosomes, most notably Trypanosoma brucei brucei, the causative agent of a wasting disease in cattle. Mechanistically, killing is initiated in the lysosome of the target trypanosome where the acidic pH facilitates a membranedisrupting activity by TLF. Here we utilize a model liposome system to characterize the membrane binding and permeabilizing activity of TLF and its protein constituents, haptoglobinrelated protein (Hpr), apolipoprotein L-1 (apoL-1), and apolipoprotein A-1 (apoA-1). We show that TLF efficiently binds and permeabilizes unilamellar liposomes at lysosomal pH, whereas non-lytic human HDL exhibits inefficient permeabilizing activity. Purified, delipidated Hpr and apoL-1 both efficiently permeabilize lipid bilayers at low pH. Trypanosome lytic factor, apoL-1, and apoA-1 exhibit specificity for anionic membranes, whereas Hpr permeabilizes both anionic and zwitterionic membranes. Analysis of the relative particle sizes of susceptible liposomes reveals distinctly different membrane-active behavior for native TLF and the delipidated protein components. We propose that lysosomal membrane damage in TLF-susceptible trypanosomes is initiated by the stable association of the TLF particle with the lysosomal membrane and that this is a property unique to this subclass of human HDL.

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“…In vivo studies in both mice and rats have demonstrated that both HDL and apoA-I can reduce leukocyte adhesion and protect the animal from the normal effects of LPS, largely thought to be mediated via the protein component of HDL (i.e. apoA-I) [73][74][75][76]. It was also discovered that patients with low plasma concentrations of HDL are more susceptible to the effects of endotoxin.…”

Section: Leukocytesmentioning

confidence: 99%

The Anti Inflammatory Effects of High Density Lipoproteins

Murphy¹,

Chin-Dusting²,

Sviridov

et al. 2009

CMC

107

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It is well recognised that increased levels of high density lipoprotein (HDL) protect against atherosclerosis and correlate with improved prognosis for vascular disease associated events. While many of the atheroprotective effects of HDL are ascribed to the ability to remove cholesterol from the vasculature through the reverse cholesterol transport system, recent work has shown that HDL may be atheroprotective through its other functions, such as regulation of endothelial adhesion molecule expression, stimulation of endothelial nitric oxide synthase and inhibition of the damaging effects of oxidised low density lipoproteins. Recently, HDL has also been described to interact with circulating cells inhibiting both leukocyte and platelet activation, therefore having further systemic anti-inflammatory functions. This review summarises the studies and models used to examine the anti-inflammatory effects of HDL and details data describing the ability to inhibit leukocyte activation, contributing to the hypothesis that raised HDL is beneficial in the context of inflammation in atherosclerosis. Further, HDL modification in disease and current therapeutic strategies such as reconstituted HDL particles and apoA I mimetic peptides is discussed to provide insights to the potential applicability of raising HDL to regress cardiovascular disease.

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Effects of human apolipoprotein A-I on endotoxin-induced leukocyte adhesion on endothelial cells in vivo and on the growth of Escherichia coli in vitro

Abstract: These data suggest that apo A-I of HDL can directly interact with endotoxin, ameliorating its effect and that apo A-I may have a direct toxic effect on whole bacteria. Therefore, therapeutic use of apo A-I in septicemia and bacterial infection should be further explored.

Cited by 19 publications

References 32 publications

High Density Lipoprotein: Assembly, Structure, Cargo, and Functions

High Density Lipoprotein: Assembly, Structure, Cargo, and Functions

Membrane Permeabilization by Trypanosome Lytic Factor, a Cytolytic Human High Density Lipoprotein

The Anti Inflammatory Effects of High Density Lipoproteins

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