We are analyzing https://link.springer.com/article/10.1186/s13075-015-0903-z.

Title:
High-mobility group box 1 potentiates antineutrophil cytoplasmic antibody-inducing neutrophil extracellular traps formation | Arthritis Research & Therapy
Description:
Recent studies found that the circulating high-mobility group box 1 (HMGB1) levels could reflect the disease activity of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). HMGB1 could prime neutrophils by increasing ANCA antigens translocation for ANCA-mediated respiratory burst and degranulation. The current study aimed to investigate whether HMGB1 participates in ANCA-induced neutrophil extracellular traps (NETs) formation, which is one of the most important pathogenic aspects in the development of AAV. NETs were induced by treating neutrophils with HMGB1 and ANCA-positive IgG in vitro. NETs formation was assessed using immunofluorescence microscopy and fluorescence probe. Antagonist for relevant receptors Toll-like receptor (TLR)2, TLR4 and the receptor for advanced glycation end products (RAGE), as well as NADPH oxidase molecules were employed. The percentage of NETs formation was significantly higher in neutrophils stimulated with HMGB1 plus ANCA-positive IgG than that in neutrophils incubated with HMGB1 or ANCA-positive IgG alone. Consistently, compared with the nonstimulated neutrophils, the cell-free DNA (cfDNA) concentration of NETs was significantly increased from 334.09 ± 46.89 ng/ml to 563.32 ± 122.07 ng/ml in the neutrophils incubated with HMGB1 plus MPO-ANCA-positive IgG (P < 0.001), and from 303.44 ± 37.14 ng/ml to 563.79 ± 145.94 ng/ml in the neutrophils incubated with HMGB1 plus PR3-ANCA-positive IgG (P < 0.001). The aforementioned effect was significantly attenuated by antagonist for relevant receptors TLR2, TLR4 and RAGE, as well as blocking NADPH oxidase. HMGB1 can potentiate ANCA-inducing NETs formation and may be involved in the pathogenesis of AAV. HMGB1 exerts effects on NETs formation through interaction with TLR2, TLR4 and RAGE, and the process is NADPH oxidase dependent.
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Keywords {🔍}

hmgb, nets, neutrophils, formation, igg, pubmed, article, tlr, google, scholar, ngml, cas, neutrophil, extracellular, antibody, rage, study, incubated, mpoancapositive, cytoplasmic, anca, dna, antineutrophil, prancapositive, group, box, preincubating, central, traps, min, vasculitis, chen, wang, aav, ancapositive, concentration, highmobility, nadph, percentage, oxidase, dependent, fig, antibodies, receptor, cells, myeloperoxidase, showed, presence, usa, antitlr,

Topics {✒️}

nf-kappab/cyclin d1 pathway anti-cit-histone h3 antibodies anti-neutrophil cytoplasmic autoantibody anca-igg-inducing nets formation patient-derived anca-positive igg antineutrophil cytoplasmic antibody antineutrophil cytoplasmic autoantibody neutrophil extracellular traps extracellular matrix-based mechanism active mpo-anca-positive vasculitis active pr3-anca-positive vasculitis autoimmune small-vessel vasculitis purified anti-human cd282 hmgb1-inducing nets formation measuring cell-free dna article download pdf anca-induced nets formation mpo-anca-positive igg pr3-anca-positive igg cell-free dna concentration potent pro-inflammatory actions full access anti-human myeloperoxidase antibodies extracellular hmgb1 induces molecular structure-functional activity anca-mediated respiratory burst hmgb1-promoted nets formation inducing pro-inflammatory neutrophil-induced injury phorbol myristate acetate research histone h3 complex cell-free dna arthritis care res arthritis res ther physiol cell physiol signaling molecules involved anti-mpo iggs nets formation induced high hmgb1 level anti-tlr2 antibody anca-positive igg anti-tlr4 antibody antineutrophilic cytoplasmatic antibody privacy choices/manage cookies rapid nets formation related subjects active pr3-anca recent studies found mouse mesangial cells

Questions {❓}

HMGB1 in cancer: good, bad, or both?
Is serum HMGB1 a biomarker in ANCA-associated vasculitis?
NETosis: how vital is it?

Schema {🗺️}

WebPage:
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         headline:High-mobility group box 1 potentiates antineutrophil cytoplasmic antibody-inducing neutrophil extracellular traps formation
         description:Recent studies found that the circulating high-mobility group box 1 (HMGB1) levels could reflect the disease activity of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). HMGB1 could prime neutrophils by increasing ANCA antigens translocation for ANCA-mediated respiratory burst and degranulation. The current study aimed to investigate whether HMGB1 participates in ANCA-induced neutrophil extracellular traps (NETs) formation, which is one of the most important pathogenic aspects in the development of AAV. NETs were induced by treating neutrophils with HMGB1 and ANCA-positive IgG in vitro. NETs formation was assessed using immunofluorescence microscopy and fluorescence probe. Antagonist for relevant receptors Toll-like receptor (TLR)2, TLR4 and the receptor for advanced glycation end products (RAGE), as well as NADPH oxidase molecules were employed. The percentage of NETs formation was significantly higher in neutrophils stimulated with HMGB1 plus ANCA-positive IgG than that in neutrophils incubated with HMGB1 or ANCA-positive IgG alone. Consistently, compared with the nonstimulated neutrophils, the cell-free DNA (cfDNA) concentration of NETs was significantly increased from 334.09 ± 46.89 ng/ml to 563.32 ± 122.07 ng/ml in the neutrophils incubated with HMGB1 plus MPO-ANCA-positive IgG (P < 0.001), and from 303.44 ± 37.14 ng/ml to 563.79 ± 145.94 ng/ml in the neutrophils incubated with HMGB1 plus PR3-ANCA-positive IgG (P < 0.001). The aforementioned effect was significantly attenuated by antagonist for relevant receptors TLR2, TLR4 and RAGE, as well as blocking NADPH oxidase. HMGB1 can potentiate ANCA-inducing NETs formation and may be involved in the pathogenesis of AAV. HMGB1 exerts effects on NETs formation through interaction with TLR2, TLR4 and RAGE, and the process is NADPH oxidase dependent.
         datePublished:2016-01-06T00:00:00Z
         dateModified:2016-01-06T00:00:00Z
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            High-mobility group box 1
            ANCA
            Neutrophil extracellular traps
            Rheumatology
            Orthopedics
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      headline:High-mobility group box 1 potentiates antineutrophil cytoplasmic antibody-inducing neutrophil extracellular traps formation
      description:Recent studies found that the circulating high-mobility group box 1 (HMGB1) levels could reflect the disease activity of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). HMGB1 could prime neutrophils by increasing ANCA antigens translocation for ANCA-mediated respiratory burst and degranulation. The current study aimed to investigate whether HMGB1 participates in ANCA-induced neutrophil extracellular traps (NETs) formation, which is one of the most important pathogenic aspects in the development of AAV. NETs were induced by treating neutrophils with HMGB1 and ANCA-positive IgG in vitro. NETs formation was assessed using immunofluorescence microscopy and fluorescence probe. Antagonist for relevant receptors Toll-like receptor (TLR)2, TLR4 and the receptor for advanced glycation end products (RAGE), as well as NADPH oxidase molecules were employed. The percentage of NETs formation was significantly higher in neutrophils stimulated with HMGB1 plus ANCA-positive IgG than that in neutrophils incubated with HMGB1 or ANCA-positive IgG alone. Consistently, compared with the nonstimulated neutrophils, the cell-free DNA (cfDNA) concentration of NETs was significantly increased from 334.09 ± 46.89 ng/ml to 563.32 ± 122.07 ng/ml in the neutrophils incubated with HMGB1 plus MPO-ANCA-positive IgG (P < 0.001), and from 303.44 ± 37.14 ng/ml to 563.79 ± 145.94 ng/ml in the neutrophils incubated with HMGB1 plus PR3-ANCA-positive IgG (P < 0.001). The aforementioned effect was significantly attenuated by antagonist for relevant receptors TLR2, TLR4 and RAGE, as well as blocking NADPH oxidase. HMGB1 can potentiate ANCA-inducing NETs formation and may be involved in the pathogenesis of AAV. HMGB1 exerts effects on NETs formation through interaction with TLR2, TLR4 and RAGE, and the process is NADPH oxidase dependent.
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      dateModified:2016-01-06T00:00:00Z
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         High-mobility group box 1
         ANCA
         Neutrophil extracellular traps
         Rheumatology
         Orthopedics
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