Blood Purification Therapies Using Dextran Sulfate Cellulose Columns Liposorber and Selesorb

Asahi, Takashi; Yamamoto, Takashi; Kutsuki, Hidetoshi

doi:10.1046/j.1526-0968.2003.00018.x

Cited by 22 publications

(13 citation statements)

References 17 publications

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“…Liposorber apheresis is an FDA-approved method for removing Apo-lipoprotein B-100-bearing low-density and very-low-density lipoprotein (LDL, vLDL) particles from the circulation in patients with familial hypercholesterolemia [11]. Highly potent neurotoxic autoantibodies were previously reported in an adult type 1 diabetes patient suffering with recurrent small vessel stroke, severe retinopathy, and dementia [9].…”

Section: Purification Of Neurotoxic Diabetic Pdand Dementia Plasma Autmentioning

confidence: 99%

Circulating Neurotoxic 5-HT2A Receptor Agonist Autoantibodies in Adult Type 2 Diabetes with Parkinson’s Disease

Zimering¹

2018

JED

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Aims: To test whether circulating neurotoxic autoantibodies increase in adult type 2 diabetes mellitus with Parkinson's disease (PD) or dementia. To identify the G-protein coupled receptor on neuroblastoma cells mediating neural inhibitory effects in diabetic Parkinson's disease plasma autoantibodies. To determine the mechanism of accelerated neuroblastoma cell death and acute neurite retraction induced by diabetic Parkinson's disease and dementia autoantibodies.Methods: Protein-A eluates from plasma of twelve older adult male diabetic patients having Parkinson's disease (n=10) or dementia (n=2), and eight age-matched control diabetic patients were tested for ability to cause accelerated N2A neuroblastoma cell death and acute neurite retraction. Specific antagonists of G protein coupled receptors belonging to the G alpha q subfamily of heterotrimetric G-proteins, the phospholipase C/inositol triphosphate/Ca2+ pathway, or the RhoA/Rho kinase pathway were tested for ability to block diabetic Parkinson's disease/dementia autoantibodyinduced neurite retraction or N2A accelerated cell loss. Sequential Liposorber LA-15 dextran sulfate cellulose/protein-A affinity chromatography was used to obtain highly-purified fractions of diabetic Parkinson's disease autoantibodies .Results: Mean accelerated neuroblastoma cell loss induced by diabetic Parkinson's disease or dementia autoantibodies significantly exceeded (P = 0.001) the level of N2A cell loss induced by an identical concentration of the diabetic autoantibodies in control patients without these two comorbid neurodegenerative disorders. Co-incubation of diabetic Parkinson's disease and dementia autoantibodies with two-hundred nanomolar concentrations of M100907, a highly selective 5-HT2AR antagonist, completely prevented autoantibody-induced accelerated N2A cell loss and neurite retraction. A higher concentration (500 nM-10μM) of alpha-1 adrenergic, angiotensin II type 1, or endothelin A receptor antagonists did not substantially inhibit autoantibody-induced neuroblastoma cell death or prevent neurite retraction. Antagonists of the inositol triphosphate receptor (2-APB, 50μM), the intracellular calcium chelator (BAPTA-AM, 30 μM) and Y27632 (10 μM), a selective RhoA/Rho kinase inhibitor, each completely blocked acute neurite retraction induced by sixty nanomolar concentrations of diabetic Parkinson's disease autoantibodies. Co-incubation with 2-APB (1-2 μM) for 8 hours' prevented autoantibody-induced N2A cell loss. The highly-purified fraction obtained after Liposorber LA/protein-A affinity chromatography in hypertriglyceridemic diabetic dementia and Parkinson's disease plasmas had apparent MWs > 30 kD, and displayed enhanced N2A toxicity requiring substantially higher concentrations of 5-HT2AR antagonists (M100907, ketanserin, spiperone) to effectively neutralize. Conclusion:These data suggest increased autoantibodies in older adult diabetes with Parkinson's disease or dementia cause accelerated neuron loss via the 5-hydroxytryptamine 2 receptor coupled to ino...

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Section: Purification Of Neurotoxic Diabetic Pdand Dementia Plasma Autmentioning

confidence: 99%

Circulating Neurotoxic 5-HT2A Receptor Agonist Autoantibodies in Adult Type 2 Diabetes with Parkinson’s Disease

Zimering¹

2018

JED

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“…This kind of columns can adsorb pathogenic anti-DNA subgroups of high avidity and/or cationic antibodies, anticardiolipin, anti-CLbeta2GPI, and anaphylatoxins (Asahi et al, 2003). Patients with active SLE showed significantly higher titers of high-avidity antidsDNA antibody than did those with inactive SLE, and their titers were significantly reduced by immunoadsorption procedures (Hashimoto et al, 1991;Braun et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Elevated levels of serum antibodies against alpha-1, 6-glucan in patients with systemic lupus erythematosus or rheumatoid arthritis

Dai

Gao²

2011

Protein Cell

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This study was undertaken to investigate whether levels of anti-alpha-1, 6-glucan antibodies in human sera correlate with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Serum samples were collected from patients with SLE (n = 30), RA (n = 30) and healthy adult volunteers. IgG, IgA and IgM levels against alpha-1, 6-glucan were measured using enzyme linked immunosorbent assays. Anti-alpha-1, 6-glucan IgG prevalence was raised in patients with active SLE (73.3%) and RA (60%) compared with healthy controls (13.3%). Strong correlation between anti-alpha-1,6-glucan-IgG levels and anti-perinuclear factor (r = 0.642; p < 0.05) in RA patients or anti-nuclear antibodies (r = 0.675; p < 0.05) in SLE patients was observed. No significant differences in anti-alpha-1,6-glucan-IgA or-IgM levels were noted between different groups. We conclude that anti-alpha-1,6-glucan-IgG levels were significantly elevated in patients with SLE or RA and positively correlated with disease activity.

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“…Another plasmaperfusion column, Selesorb (Kaneka, Osaka, Japan) which is particularly used in SLE consists of dextran sulphate immobilized to cellulose. The dextran sulphate adsorber predominantly removes anti-DNA and anti-cardiolipin auto-Ab through electrostatic bonding between the negatively charged adsorbent and the Fab fragments of the autoantibodies, probably including positively charged aminoacids [28]. More recently developed adsorber systems contain synthetic peptides covalently bound to a sepharose matrix as ligands for human Ig.…”

Section: Adsorber Systemsmentioning

confidence: 99%

Immunoadsorption in pemphigus

Eming

Hertl

2006

Autoimmunity

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The principle of extracorporal immunoadsorption (IA) is based on affinity adsorption of pathogenic (auto-)antibodies and circulating immune complexes (CIC) which reversibly bind to an immobilized ligand of the adsorber. In pemphigus, a blistering autoimmune disease affecting skin and mucous membranes, autoantibodies, mainly of the IgG subclass are directed against desmosomal adhesion molecules and other non-desmosomal antigens on the surface of epidermal keratinocytes, such as acetylcholine receptors. The pathogenicity of these autoantibodies has been shown in various in vitro and in vivo systems. Recently, IA was applied in severe pemphigus demonstrating that a rapid and dramatic decline in desmoglein (Dsg)-reactive autoantibodies is accompanied by clinical remission of mucocutaneous blisters and erosions. As an adjuvant treatment, IA was combined with systemic immunosuppressive medication and current protocols initially apply treatment cycles of 3-4 IAs on consecutive days followed by immunoapheresis once a week or repeating the initial cycle in 4 week intervals depending on the disease activity. IA in pemphigus is generally safe and well tolerated.

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Blood Purification Therapies Using Dextran Sulfate Cellulose Columns Liposorber and Selesorb

Cited by 22 publications

References 17 publications

Circulating Neurotoxic 5-HT2A Receptor Agonist Autoantibodies in Adult Type 2 Diabetes with Parkinson’s Disease

Circulating Neurotoxic 5-HT2A Receptor Agonist Autoantibodies in Adult Type 2 Diabetes with Parkinson’s Disease

Elevated levels of serum antibodies against alpha-1, 6-glucan in patients with systemic lupus erythematosus or rheumatoid arthritis

Immunoadsorption in pemphigus

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