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[PMID]:28682564
[Au] Autor:Visconti L; Cernaro V; Ardissino G; Sgarbanti M; Ferrara D; Visconti G; Santoro D; Buemi M
[Ad] Endereço:Cattedra di Nefrologia, Dipartimento di Medicina clinica e sperimentale, Università di Messina, Messina, Italia.
[Ti] Título:[Complement factor B mutation in atypical hemolytic uremic syndrome. Rare cause of rare disease].
[So] Source:G Ital Nefrol;34(2):74-81, 2017 Apr.
[Is] ISSN:1724-5990
[Cp] País de publicação:Italy
[La] Idioma:ita
[Ab] Resumo:Hemolytic uremic syndrome (HUS) is a rare disease characterized by microangiopathic hemolysis, platelet consumption and multiple organ failure with predominant renal involvement. In the most of cases (85-90%), it is associated with enteric infection due to Shiga-toxin or verocytotoxin (STEC-VTEC)-producer Escherichia coli. Rarely, in about 10-15% of cases, HUS develops in the presence of a disorder of alternative complement pathway regulation and it is defined atypical (aHUS). We describe the case of a 65-year-old man who came to our attention with a clinical presentation of aHUS and a clinical course characterized by rapidly progressive acute renal failure (ARF), which required renal replacement treatments, and by a stable clinical picture of hematological impairment as a marker of a non-severe and self-limiting form. The clinical and laboratory course allowed us not to perform specific therapies such as plasma exchange and/or block of the complement with eculizumab. Less than two weeks after hospital admission, there was a gradual recovery of renal function with spontaneous diuresis and hematological remission. Genetic screening has revealed a heterozygous mutation in the complement factor B (CFB) that is not described in the literature and therefore not yet characterized in the genotype/phenotype correlation, also for the extreme rarity of the forms associated with CFB alteration. In conclusion, the presence of a new mutation in the CFB, such as the one described in our case, is probably associated with the development of aHUS but has not led to a poor prognosis, as generally reported in the literature for known variants of the CFB.
[Mh] Termos MeSH primário: Síndrome Hemolítico-Urêmica Atípica/genética
Fator B do Complemento/genética
Mutação
Doenças Raras/genética
[Mh] Termos MeSH secundário: Idoso
Seres Humanos
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.21.47 (Complement Factor B)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE


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[PMID]:28662037
[Au] Autor:Chun N; Haddadin AS; Liu J; Hou Y; Wong KA; Lee D; Rushbrook JI; Gulaya K; Hines R; Hollis T; Nistal Nuno B; Mangi AA; Hashim S; Pekna M; Catalfamo A; Chin HY; Patel F; Rayala S; Shevde K; Heeger PS; Zhang M
[Ad] Endereço:Nephrology Division, Department of Medicine and Translational Transplant Research Center, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
[Ti] Título:Activation of complement factor B contributes to murine and human myocardial ischemia/reperfusion injury.
[So] Source:PLoS One;12(6):e0179450, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The pathophysiology of myocardial injury that results from cardiac ischemia and reperfusion (I/R) is incompletely understood. Experimental evidence from murine models indicates that innate immune mechanisms including complement activation via the classical and lectin pathways are crucial. Whether factor B (fB), a component of the alternative complement pathway required for amplification of complement cascade activation, participates in the pathophysiology of myocardial I/R injury has not been addressed. We induced regional myocardial I/R injury by transient coronary ligation in WT C57BL/6 mice, a manipulation that resulted in marked myocardial necrosis associated with activation of fB protein and myocardial deposition of C3 activation products. In contrast, in fB-/- mice, the same procedure resulted in significantly reduced myocardial necrosis (% ventricular tissue necrotic; fB-/- mice, 20 ± 4%; WT mice, 45 ± 3%; P < 0.05) and diminished deposition of C3 activation products in the myocardial tissue (fB-/- mice, 0 ± 0%; WT mice, 31 ± 6%; P<0.05). Reconstitution of fB-/- mice with WT serum followed by cardiac I/R restored the myocardial necrosis and activated C3 deposition in the myocardium. In translational human studies we measured levels of activated fB (Bb) in intracoronary blood samples obtained during cardio-pulmonary bypass surgery before and after aortic cross clamping (AXCL), during which global heart ischemia was induced. Intracoronary Bb increased immediately after AXCL, and the levels were directly correlated with peripheral blood levels of cardiac troponin I, an established biomarker of myocardial necrosis (Spearman coefficient = 0.465, P < 0.01). Taken together, our results support the conclusion that circulating fB is a crucial pathophysiological amplifier of I/R-induced, complement-dependent myocardial necrosis and identify fB as a potential therapeutic target for prevention of human myocardial I/R injury.
[Mh] Termos MeSH primário: Fator B do Complemento/metabolismo
Traumatismo por Reperfusão Miocárdica/metabolismo
[Mh] Termos MeSH secundário: Idoso
Animais
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.21.47 (Complement Factor B)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170630
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179450


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[PMID]:28322200
[Au] Autor:Riihilä P; Nissinen L; Farshchian M; Kallajoki M; Kivisaari A; Meri S; Grénman R; Peltonen S; Peltonen J; Pihlajaniemi T; Heljasvaara R; Kähäri VM
[Ad] Endereço:Department of Dermatology, University of Turku and Turku University Hospital, Turku, Finland; MediCity Research Laboratory, University of Turku, Turku, Finland.
[Ti] Título:Complement Component C3 and Complement Factor B Promote Growth of Cutaneous Squamous Cell Carcinoma.
[So] Source:Am J Pathol;187(5):1186-1197, 2017 May.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cutaneous squamous cell carcinoma (cSCC) is one of the most common metastatic skin cancers with increasing incidence. We examined the roles of complement component C3 and complement factor B (CFB) in the growth of cSCC. Analysis of cSCC cell lines (n = 8) and normal human epidermal keratinocytes (n = 11) with real-time quantitative PCR and Western blotting revealed up-regulation of C3 and CFB expression in cSCC cells. Immunohistochemical staining revealed stronger tumor cell-specific labeling for C3 and CFB in invasive cSCCs (n = 71) and recessive dystrophic epidermolysis bullosa-associated cSCCs (n = 11) than in cSCC in situ (n = 69), actinic keratoses (n = 63), and normal skin (n = 5). Significant up-regulation of C3 and CFB mRNA expression was noted in chemically induced mouse cSCCs, compared to benign papillomas. Knockdown of C3 and CFB expression inhibited migration and proliferation of cSCC cells and resulted in potent inhibition of extracellular signal-regulated kinase 1/2 activation. Knockdown of C3 and CFB markedly inhibited growth of human cSCC xenograft tumors in vivo. These results provide evidence for the roles of C3 and CFB in the development of cSCC and identify them as biomarkers and potential therapeutic targets in this metastatic skin cancer.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/etiologia
Complemento C3/fisiologia
Fator B do Complemento/fisiologia
Neoplasias Cutâneas/etiologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Animais
Carcinogênese
Estudos de Casos e Controles
Linhagem Celular Tumoral
Movimento Celular/fisiologia
Proliferação Celular/fisiologia
Complemento C3/metabolismo
Fator B do Complemento/metabolismo
Feminino
Xenoenxertos
Seres Humanos
Camundongos Endogâmicos A
Camundongos Nus
Meia-Idade
Transplante de Neoplasias/métodos
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Complement C3); EC 3.4.21.47 (Complement Factor B)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE


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[PMID]:28130094
[Au] Autor:Li XP; Sun L
[Ad] Endereço:Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, Qingdao, China; University of Chinese Academy of Sciences, Beijing, China.
[Ti] Título:A teleost complement factor Ba possesses antimicrobial activity and inhibits bacterial infection in fish.
[So] Source:Dev Comp Immunol;71:49-58, 2017 06.
[Is] ISSN:1879-0089
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Complement factor B (Bf) is a component of the complement system. Following activation of the alternative pathway of the complement system, factor B is cleaved into Ba and Bb fragments. In fish, the Bf of rainbow trout is known to act as a C3 convertase, but the function of the Ba fragment is essentially unknown. In this study, we examined the expression patterns of tongue sole Cynoglossus semilaevis Bf (named CsBf) and the biological activity of the Ba fragment of CsBf (named CsBa). CsBf possesses the conserved domains of Bf and shares 39.9%-56.4% sequence identities with other fish Bf. CsBf expression was high in liver, muscle, and heart, and low in intestine, blood, and kidney. Bacterial infection significantly induced CsBf expression in kidney, spleen, and liver in a time-dependent manner. Recombinant CsBa (rCsBa) exhibited apparent binding capacities to bacteria and tongue sole peripheral blood leukocytes, and binding of rCsBa to bacteria inhibited bacterial growth. When overexpressed in tongue sole, CsBa significantly reduced bacterial dissemination in fish tissues. Together these results indicate for the first time that a fish Ba possesses antibacterial effect as well as immune cell-binding capacity, and thus probably plays a role in host immune defense against bacterial infection.
[Mh] Termos MeSH primário: Fator B do Complemento/metabolismo
Edwardsiella/imunologia
Proteínas de Peixes/metabolismo
Linguados/imunologia
Infecções por Bactérias Gram-Negativas/imunologia
Pseudomonas/imunologia
Vibrio/imunologia
[Mh] Termos MeSH secundário: Animais
Anti-Infecciosos/metabolismo
Carga Bacteriana
Processos de Crescimento Celular
Clonagem Molecular
Fator B do Complemento/genética
Via Alternativa do Complemento
Proteínas de Peixes/genética
Expressão Gênica
Infecções por Bactérias Gram-Negativas/terapia
Imunidade Inata
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Infective Agents); 0 (Fish Proteins); EC 3.4.21.47 (Complement Factor B)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170129
[St] Status:MEDLINE


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[PMID]:28096309
[Au] Autor:Marinozzi MC; Roumenina LT; Chauvet S; Hertig A; Bertrand D; Olagne J; Frimat M; Ulinski T; Deschênes G; Burtey S; Delahousse M; Moulin B; Legendre C; Frémeaux-Bacchi V; Le Quintrec M
[Ad] Endereço:Team Complement and Diseases Cordeliers Research Center, Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche 1138, Paris, France.
[Ti] Título:Anti-Factor B and Anti-C3b Autoantibodies in C3 Glomerulopathy and Ig-Associated Membranoproliferative GN.
[So] Source:J Am Soc Nephrol;28(5):1603-1613, 2017 May.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In C3 glomerulopathy (C3G), the alternative pathway of complement is frequently overactivated by autoantibodies that stabilize the C3 convertase C3bBb. Anti-C3b and anti-factor B (anti-FB) IgG have been reported in three patients with C3G. We screened a cohort of 141 patients with C3G and Ig-associated membranoproliferative GN (Ig-MPGN) for anti-FB and anti-C3b autoantibodies using ELISA. We identified seven patients with anti-FB IgG, three patients with anti-C3b IgG, and five patients with anti-FB and anti-C3b IgG. Of these 15 patients, ten were diagnosed with Ig-MPGN. Among those patients with available data, 92% had a nephrotic syndrome, 64% had AKI, and 67% had a documented infection. Patients negative for anti-C3b and anti-FB IgG had much lower rates of infection (17 [25%] patients with C3G and one [10%] patient with Ig-MPGN). After 48 months, four of 15 (26%) positive patients had developed ESRD or died. All 15 patients had high plasma Bb levels, six (40%) patients had low levels of C3, and nine (60%) patients had high levels of soluble C5b9. , IgG purified from patients with anti-FB Abs selectively enhanced C3 convertase activity; IgG from patients with anti-C3b/anti-FB Abs enhanced C3 and C5 cleavage. IgG from patients with anti-C3b Abs stabilized C3bBb and perturbed C3b binding to complement receptor 1 but did not perturb binding to factor H. In conclusion, the prevalence of anti-C3b/anti-FB Abs and alternative pathway activation is similar in Ig-MPGN and C3G, suggesting similar pathogenic mechanisms. Identification of the underlying defect in Ig-MPGN could lead to improved treatment.
[Mh] Termos MeSH primário: Autoanticorpos/imunologia
Complemento C3b/imunologia
Fator B do Complemento/imunologia
Glomerulonefrite Membranoproliferativa/imunologia
Imunoglobulina G/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Retrospectivos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Immunoglobulin G); 80295-43-8 (Complement C3b); EC 3.4.21.47 (Complement Factor B)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170531
[Lr] Data última revisão:
170531
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170119
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2016030343


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[PMID]:27913792
[Au] Autor:Mizumura H; Ogura N; Aketagawa J; Aizawa M; Kobayashi Y; Kawabata SI; Oda T
[Ad] Endereço:1 LAL Research and Development Department, Seikagaku Corporation, Tokyo, Japan.
[Ti] Título:Genetic engineering approach to develop next-generation reagents for endotoxin quantification.
[So] Source:Innate Immun;23(2):136-146, 2017 Feb.
[Is] ISSN:1753-4267
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The bacterial endotoxin test, which uses amebocyte lysate reagents of horseshoe crab origin, is a sensitive, reproducible and simple assay to measure endotoxin concentration. To develop sustainable raw materials for lysate reagents that do not require horseshoe crabs, three recombinant protease zymogens (factor C, derived from mammalian cells; factor B; and the proclotting enzyme derived from insect cells) were prepared using a genetic engineering technique. Recombinant cascade reagents (RCRs) were then prepared to reconstruct the reaction cascade in the amebocyte lysate reagent. The protease activity of the RCR containing recombinant factor C was much greater than that of recombinant factor C alone, indicating the efficiency of signal amplification in the cascade. Compared with the RCR containing the insect cell-derived factor C, those containing mammalian cell-derived factor C, which features different glycosylation patterns, were less susceptible to interference by the injectable drug components. The standard curve of the RCR containing mammalian cell-derived recombinant factor C had a steeper slope than the curves for those containing natural lysate reagents, suggesting a greater sensitivity to endotoxin. The present study supports the future production of recombinant reagents that do not require the use of natural resources.
[Mh] Termos MeSH primário: Fator B do Complemento/metabolismo
Endopeptidases/metabolismo
Endotoxinas/análise
Precursores Enzimáticos/metabolismo
Proteínas de Insetos/metabolismo
Teste do Limulus/métodos
Serina Endopeptidases/metabolismo
[Mh] Termos MeSH secundário: Animais
Extratos Celulares
Fator B do Complemento/genética
Endopeptidases/genética
Precursores Enzimáticos/genética
Engenharia Genética
Caranguejos Ferradura
Indicadores e Reagentes
Proteínas de Insetos/genética
Proteínas Recombinantes/genética
Padrões de Referência
Sensibilidade e Especificidade
Serina Endopeptidases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Extracts); 0 (Endotoxins); 0 (Enzyme Precursors); 0 (Indicators and Reagents); 0 (Insect Proteins); 0 (Recombinant Proteins); EC 3.4.- (Endopeptidases); EC 3.4.21.- (Serine Endopeptidases); EC 3.4.21.47 (Complement Factor B); EC 3.4.99.- (pro-clotting enzyme)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161204
[St] Status:MEDLINE
[do] DOI:10.1177/1753425916681074


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[PMID]:27824510
[Au] Autor:Laliotis GP; Marantidis A; Avdi M
[Ad] Endereço:a Laboratory of Physiology of Reproduction of Farm Animals, Department of Animal Production, School of Agriculture , Aristotle University of Thessaloniki , Thessaloniki , Greece.
[Ti] Título:Association of BF, RBP4, and ESR2 Genotypes with Litter Size in an Autochthonous Pig Population.
[So] Source:Anim Biotechnol;28(2):138-143, 2017 Apr 03.
[Is] ISSN:1532-2378
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The aim of the present study was to determine any potential association of the BF, RBP4, and ESR2 genes with reproduction traits in an autochthonous Greek pig population. The PCR-RFLP methodology was implemented for genotyping purposes of the examined genes. No deviation from the Hardy-Weinberg equilibrium was observed for the examined loci, while the B allele noted to be the more frequent in all analyzed genes. In addition, sows with the AA genotype of BF gene found to produce significantly lower numbers of the total born piglets (TNB) and number of piglets born alive (TNA), while the respective BB genotype significantly exceeded in TNB and NBA traits compared to the other two genotypes (P < 0.001). In the case of RBP4 gene, sows with the AB genotype noted to have significant higher values of TNB and NBA in regard to the respective homozygous genotypes (AA or BB), while the BB genotype showed intermediate results (P < 0.001). There were no statistical differences between the BB genotype and the AB genotype of ESR2 locus in regard to the examined traits. However, a noticeable superiority (P < 0.01) of the BB genotype compared to the homozygous AA genotype, adding almost 2 piglets/litter in TNB and NBA trait, was found. ABBREVIATIONS: TNB: Total number of born piglets; NBA: Number of piglets born alive.
[Mh] Termos MeSH primário: Fator B do Complemento/genética
Receptor beta de Estrogênio/genética
Tamanho da Ninhada de Vivíparos/genética
Resultado da Gravidez/genética
Resultado da Gravidez/veterinária
Suínos/genética
[Mh] Termos MeSH secundário: Animais
Feminino
Estudos de Associação Genética/métodos
Estudos de Associação Genética/veterinária
Predisposição Genética para Doença/epidemiologia
Predisposição Genética para Doença/genética
Genótipo
Grécia/epidemiologia
Masculino
Polimorfismo de Nucleotídeo Único/genética
Gravidez
Resultado da Gravidez/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor beta); EC 3.4.21.47 (Complement Factor B)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170619
[Lr] Data última revisão:
170619
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161109
[St] Status:MEDLINE
[do] DOI:10.1080/10495398.2016.1242490


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[PMID]:27759029
[Au] Autor:Gupta A; Juyal G; Sood A; Midha V; Yamazaki K; Vich Vila A; Esaki M; Matsui T; Takahashi A; Kubo M; Weersma RK; Thelma BK
[Ad] Endereço:Department of Genetics, University of Delhi South Campus, New Delhi, India.
[Ti] Título:A cross-ethnic survey of CFB and SLC44A4, Indian ulcerative colitis GWAS hits, underscores their potential role in disease susceptibility.
[So] Source:Eur J Hum Genet;25(1):111-122, 2016 Jan.
[Is] ISSN:1476-5438
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The first ever genome-wide association study (GWAS) of ulcerative colitis in genetically distinct north Indian population identified two novel genes namely CFB and SLC44A4. Considering their biological relevance, we investigated allelic/genetic heterogeneity in these genes among ulcerative colitis cohorts of north Indian, Japanese and Dutch origin using high-density ImmunoChip case-control genotype data. Comparative linkage disequilibrium profiling and test of association were performed. Of the 28 CFB SNPs, similar strength of association was observed for rs4151657 (novel ulcerative colitis GWAS SNP) in north Indians (P=1.73 × 10 ) and Japanese (P=2.02 × 10 ) but not in the Dutch. Further, a three-marker haplotype was shared between north Indians and Japanese (P<10 ), but a different five-marker haplotype was associated (P=2.07 × 10 ) in the Dutch. Of the 22 SLC44A4 SNPs, rs2736428 (novel ulcerative colitis GWAS SNP) was found significantly associated in north Indians (P=4.94 × 10 ) and Japanese (P=3.37 × 10 ), but not among the Dutch. These results suggest (i) apparent allelic heterogeneity in CFB and genetic heterogeneity in SLC44A4 across different ethnic groups; (ii) shared ulcerative colitis genetic etiological factors among Asians; and finally (iii) re-exploration of GWAS findings together with high-density genotyping/sequencing and trans-ethnic fine mapping approaches may help identify shared and population-specific risk variants and enable to explain missing disease heritability.
[Mh] Termos MeSH primário: Colite Ulcerativa/genética
Fator B do Complemento/genética
Predisposição Genética para Doença
Proteínas de Membrana Transportadoras/genética
[Mh] Termos MeSH secundário: Colite Ulcerativa/epidemiologia
Colite Ulcerativa/patologia
Grupos Étnicos/genética
Feminino
Estudo de Associação Genômica Ampla
Genótipo
Seres Humanos
Japão
Desequilíbrio de Ligação
Masculino
Países Baixos
Polimorfismo de Nucleotídeo Único
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Transport Proteins); 0 (choline transporter-like protein 4, human); EC 3.4.21.47 (Complement Factor B)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE
[do] DOI:10.1038/ejhg.2016.131


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[PMID]:27662014
[Au] Autor:Cao W; Pham HP; Williams LA; McDaniel J; Siniard RC; Lorenz RG; Marques MB; Zheng XL
[Ad] Endereço:Division of Laboratory Medicine, Department of Pathology, University of Alabama at Birmingham, AL, USA.
[Ti] Título:Human neutrophil peptides and complement factor Bb in pathogenesis of acquired thrombotic thrombocytopenic purpura.
[So] Source:Haematologica;101(11):1319-1326, 2016 Nov.
[Is] ISSN:1592-8721
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Acquired thrombotic thrombocytopenic purpura is primarily caused by the deficiency of plasma ADAMTS13 activity resulting from autoantibodies against ADAMTS13. However, ADAMTS13 deficiency alone is often not sufficient to cause acute thrombotic thrombocytopenic purpura. Infections or systemic inflammation may precede acute bursts of the disease, but the underlying mechanisms are not fully understood. Herein, 52 patients with acquired autoimmune thrombotic thrombocytopenic purpura and 30 blood donor controls were recruited for the study. The plasma levels of human neutrophil peptides 1-3 and complement activation fragments (i.e. Bb, iC3b, C4d, and sC5b-9) were determined by enzyme-linked immunosorbent assays. Univariate analyses were performed to determine the correlation between each biomarker and clinical outcomes. We found that the plasma levels of human neutrophil peptides 1-3 and Bb in patients with acute thrombotic thrombocytopenic purpura were significantly higher than those in the control (P<0.0001). The plasma levels of HNP1-3 correlated with the levels of plasma complement fragment Bb (rho=0.48, P=0.0004) and serum lactate dehydrogenase (rho=0.28, P=0.04); in addition, the plasma levels of Bb correlated with iC3b (rho=0.55, P<0.0001), sC5b-9 (rho=0.63, P<0.0001), serum creatinine (rho=0.42, p=0.0011), and lactate dehydrogenase (rho=0.40, P=0.0034), respectively. Moreover, the plasma levels of iC3b and sC5b-9 were correlated (rho=0.72, P<0.0001), despite no statistically significant difference of the two markers between thrombotic thrombocytopenic purpura patients and the control. We conclude that innate immunity, i.e. neutrophil and complement activation via the alternative pathway, may play a role in the pathogenesis of acute autoimmune thrombotic thrombocytopenic purpura, and a therapy targeted at these pathways may be considered in a subset of these patients.
[Mh] Termos MeSH primário: Fator B do Complemento/análise
Púrpura Trombocitopênica Trombótica/imunologia
alfa-Defensinas/sangue
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Imunidade Inata
Masculino
Púrpura Trombocitopênica Trombótica/etiologia
Púrpura Trombocitopênica Trombótica/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (alpha-Defensins); 0 (human neutrophil peptide 1); 0 (human neutrophil peptide 2); 0 (human neutrophil peptide 3); EC 3.4.21.47 (Complement Factor B)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170622
[Lr] Data última revisão:
170622
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160924
[St] Status:MEDLINE


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[PMID]:27564415
[Au] Autor:Williams JA; Stampoulis D; Gunter CE; Greenwood J; Adamson P; Moss SE
[Ad] Endereço:Department of Cell Biology, UCL Institute of Ophthalmology, 11-43 Bath Street, London EC1V 9EL, United Kingdom.
[Ti] Título:Regulation of C3 Activation by the Alternative Complement Pathway in the Mouse Retina.
[So] Source:PLoS One;11(8):e0161898, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to examine the retinas of mice carrying hemizygous and null double deletions of Cfb-/- and Cfh-/-, and to compare these with the single knockouts of Cfb, Cfh and Cfd. Retinas were isolated from wild type (WT), Cfb-/-/Cfh-/-, Cfb-/-/Cfh+/-, Cfh-/-/Cfb+/-, Cfb-/-, Cfh-/- Cfd-/-, and Cfd+/- mice. Complement proteins were evaluated by western blotting, ELISA and immunocytochemistry, and retinal morphology was assessed using toluidine blue stained semi-thin sections. WT mice showed staining for C3 and its breakdown products in the retinal vasculature and the basal surface of the retinal pigment epithelium (RPE). Cfb-/- mice exhibited a similar C3 staining pattern to WT in the retinal vessels but a decrease in C3 and its breakdown products at the basal surface of the RPE. Deletion of both Cfb and Cfh restored C3 to levels similar to those observed in WT mice, however this reversal of phenotype was not observed in Cfh-/-/Cfb+/- or Cfb-/-/Cfh+/- mice. Loss of CFD caused an increase in C3 and a decrease in C3 breakdown products along the basal surface of the RPE. Overall the retinal morphology and retinal vasculature did not appear different across the various genotypes. We observed that C3 accumulates at the basal RPE in Cfb-/-, Cfb-/-/Cfh-/-, Cfb-/-/Cfh+/-, Cfd-/- and WT mice, but is absent in Cfh-/- and Cfh-/-/Cfb+/- mice, consistent with its consumption in the serum of mice lacking CFH when CFB is present. C3 breakdown products along the surface of the RPE were either decreased or absent when CFB, CFH or CFD was deleted or partially deleted.
[Mh] Termos MeSH primário: Convertases de Complemento C3-C5/metabolismo
Via Alternativa do Complemento/fisiologia
Retina/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Complemento C5/genética
Complemento C5/metabolismo
Fator B do Complemento/genética
Fator B do Complemento/metabolismo
Fator D do Complemento/genética
Fator D do Complemento/metabolismo
Fator H do Complemento/genética
Fator H do Complemento/metabolismo
Via Alternativa do Complemento/genética
Ensaio de Imunoadsorção Enzimática
Imunofluorescência
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Mutantes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Complement C5); 80295-65-4 (Complement Factor H); EC 3.4.21.- (Complement C3-C5 Convertases); EC 3.4.21.46 (Complement Factor D); EC 3.4.21.47 (Complement Factor B)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160827
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0161898



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