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https://www.readbyqxmd.com/read/28640789/complement-mediated-enhancement-of-monocyte-adhesion-to-endothelial-cells-by-hla-antibodies-and-blockade-by-a-specific-inhibitor-of-the-classical-complement-cascade-tnt003
#1
Nicole M Valenzuela, Kimberly A Thomas, Arend Mulder, Graham C Parry, Sandip Panicker, Elaine F Reed
BACKGROUND: Antibody-mediated rejection (AMR) of most solid organs is characterized by evidence of complement activation and/or intragraft macrophages (C4d + and CD68+ biopsies). We previously demonstrated that crosslinking of HLA I by antibodies triggered endothelial activation and monocyte adhesion. We hypothesized that activation of the classical complement pathway at the endothelial cell surface by HLA antibodies would enhance monocyte adhesion through soluble split product generation, in parallel with direct endothelial activation downstream of HLA signaling...
July 2017: Transplantation
https://www.readbyqxmd.com/read/28634882/gingipain-of-porphyromonas-gingivalis-manipulates-m1-macrophage-polarization-through-c5a-pathway
#2
Yubo Hou, Haiyan Yu, Xinchan Liu, Gege Li, Jiahui Pan, Changyu Zheng, Weixian Yu
Gingipains secreted by Porphyromonas gingivalis (P. gingivalis, Pg) play an important role in maintaining macrophage infiltrating. And, this study is to evaluate effects of gingipain on M1 macrophage polarization after exposure to Porphyromonas gingivalis (P. gingivalis, Pg) and if these effects are through complement component 5a (C5a) pathway. Mouse RAW264.7 macrophages were exposed to gingipain extracts, Escherichia coli lipopolysaccharides (Ec-LPS), Pg-LPS with or without the C5aR antagonist: PMX-53 for 24 h...
June 20, 2017: In Vitro Cellular & Developmental Biology. Animal
https://www.readbyqxmd.com/read/28631067/antibodies-against-complement-components-relevance-for-the-antiphospholipid-syndrome-biomarkers-of-the-disease-and-biopharmaceuticals
#3
REVIEW
Mirjana Bećarević
PURPOSE OF REVIEW: Laboratory criterion for the diagnosis of antiphospholipid syndrome (APS) is the presence of antiphospholipid antibodies (aPL Abs). Complement system has a role in mediating aPL Abs-induced thrombosis in animal models. The importance of antibodies against complement components (potential biomarkers of APS) and the importance of antibodies with beneficial anti-complement effects in APS (as biopharmaceuticals) are reviewed. RECENT FINDINGS: Antibodies against complement components described in APS patients, so far, are anti-C1q and anti-factor H Abs, although anti-factor B Abs and anti-C5a Abs were described in animal models of APS...
July 2017: Current Rheumatology Reports
https://www.readbyqxmd.com/read/28630122/eculizumab-blocks-vaccine-induced-opsonophagocytic-killing-of-meningococci-by-whole-blood-from-immunized-adults
#4
Monica Konar, Dan M Granoff
Eculizumab, a humanized anti-complement C5 monoclonal antibody for treatment of paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome, blocks the terminal complement pathway required for serum bactericidal activity (SBA). Because treated patients are at >1000-fold increased risk of meningococcal disease, vaccination is recommended, but whether vaccination can protect by opsonophagocytic activity in the absence of SBA is not known. Meningococci were added to anticoagulated blood from 12 healthy adults vaccinated with meningococcal serogroup B and serogroup A,C,W,Y vaccines...
June 19, 2017: Blood
https://www.readbyqxmd.com/read/28628799/a-novel-2-stage-approach-that-detects-complement-activation-in-patients-with-antiphospholipid-antibody-syndrome
#5
Jacob H Rand, Xiao-Xuan Wu, Lucia R Wolgast, Victor Lei, Edward M Conway
INTRODUCTION: The antiphospholipid syndrome (APS) is marked by autoantibodies that recognize anionic phospholipids in a cofactor-dependent manner. A role for complement has been implicated in the pathophysiology, however, elevations of complement activation markers have not been consistently demonstrated in clinical studies. We therefore designed a proof-of-principle study to determine whether complement activation might be detectable in APS by first exposing plasmas to phospholipid vesicles...
June 9, 2017: Thrombosis Research
https://www.readbyqxmd.com/read/28620195/attenuation-of-cgvhd-by-c5a-c5ar-blockade-is-associated-with-increased-frequency-of-treg
#6
Yulian Wang, Peilong Lai, Xiaomei Chen, Chang He, Xin Huang, Suxia Geng, Chenwei Luo, Suijing Wu, Wei Ling, Liye Zhong, Zesheng Lu, Peng Li, Jianyu Weng, Xin Du
C5aR signaling plays an important role in the regulation of T cell activation and alloimmune responses in chronic graft-versus-host disease (cGVHD). However, direct evidence of this modulation and the efficacy of C5aR blockade in the treatment of cGVHD have not been demonstrated. We observed higher expression of C5aR on both monocytes and T cells of patients with cGVHD compared with healthy controls and non-GVHD patients after allogeneic hematopoietic stem cell transplantation. Our data also demonstrated a significant negative correlation between C5aR expression and regulatory T cells (Treg) frequency in cGVHD patients, indicating a potential role of C5aR in the generation and regulation of Treg...
June 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28614388/osteoblast-specific-overexpression-of-complement-receptor-c5ar1-impairs-fracture-healing
#7
Stephanie Bergdolt, Anna Kovtun, Yvonne Hägele, Astrid Liedert, Thorsten Schinke, Michael Amling, Markus Huber-Lang, Anita Ignatius
The anaphylatoxin receptor C5aR1 plays an important role not only in innate immune responses, but also in bone metabolism and fracture healing, being highly expressed on immune and bone cells, including osteoblasts and osteoclasts. C5aR1 induces osteoblast migration, cytokine generation and osteoclastogenesis, however, the exact role of C5aR1-mediated signaling in osteoblasts is not entirely known. Therefore, we hypothesized that osteoblasts are essential target cells for C5a and that fracture healing should be disturbed in mice with an osteoblast-specific C5aR1 overexpression (Col1a1-C5aR1)...
2017: PloS One
https://www.readbyqxmd.com/read/28611987/complement-in-kidney-transplantation
#8
REVIEW
Marek Cernoch, Ondrej Viklicky
The complement system is considered to be an important part of innate immune system with a significant role in inflammation processes. The activation can occur through classical, alternative, or lectin pathway, resulting in the creation of anaphylatoxins C3a and C5a, possessing a vast spectrum of immune functions, and the assembly of terminal complement cascade, capable of direct cell lysis. The activation processes are tightly regulated; inappropriate activation of the complement cascade plays a significant role in many renal diseases including organ transplantation...
2017: Frontiers in Medicine
https://www.readbyqxmd.com/read/28610663/eculizumab-c5-complexes-express-a-c5a-neoepitope-in-vivo-consequences-for-interpretation-of-patient-complement-analyses
#9
Per H Nilsson, Anub Mathew Thomas, Grethe Bergseth, Alice Gustavsen, Elena B Volokhina, Lambertus P van den Heuvel, Andreas Barratt-Due, Tom E Mollnes
The complement system has obtained renewed clinical focus due to increasing number of patients treated with eculizumab, a monoclonal antibody inhibiting cleavage of C5 into C5a and C5b. The FDA approved indications are paroxysmal nocturnal haemoglobinuria and atypical haemolytic uremic syndrome, but many other diseases are candidates for complement inhibition. It has been postulated that eculizumab does not inhibit C5a formation in vivo, in contrast to what would be expected since it blocks C5 cleavage. We recently revealed that this finding was due to a false positive reaction in a C5a assay...
June 10, 2017: Molecular Immunology
https://www.readbyqxmd.com/read/28606989/tlr7-8-activation-in-neutrophils-impairs-immune-complex-phagocytosis-through-shedding-of-fcgriia
#10
Christian Lood, Sabine Arve, Jeffrey Ledbetter, Keith B Elkon
Neutrophils play a crucial role in host defense. However, neutrophil activation is also linked to autoimmune diseases such as systemic lupus erythematosus (SLE), where nucleic acid-containing immune complexes (IC) drive inflammation. The role of Toll-like receptor (TLR) signaling in processing of SLE ICs and downstream inflammatory neutrophil effector functions is not known. We observed that TLR7/8 activation leads to a furin-dependent proteolytic cleavage of the N-terminal part of FcgRIIA, shifting neutrophils away from phagocytosis of ICs toward the programmed form of necrosis, NETosis...
June 12, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/28600003/novel-insights-into-the-expression-pattern-of-anaphylatoxin-receptors-in-mice-and-men
#11
Yves Laumonnier, Christian M Karsten, Jörg Köhl
The anaphylatoxins (AT) C3a and C5a play important roles as mediators of inflammation. Further, they regulate and control multiple innate and adaptive immune responses through binding and activation of their cognate G protein-coupled receptors, i.e. C3a receptor (C3aR), C5a receptor 1 (C5aR1) and C5a receptor 2 (C5aR2), although the latter lacks important sequence motifs for G protein-coupling. Based on their pleiotropic functions, they contribute not only to tissue homeostasis but drive, perpetuate and resolve immune responses in many inflammatory diseases including infections, malignancies, autoimmune as well as allergic diseases...
June 6, 2017: Molecular Immunology
https://www.readbyqxmd.com/read/28579778/iron-oxide-nanoparticles-induce-cytokine-secretion-in-a-complement-dependent-manner-in-a-human-whole-blood-model
#12
Susann Wolf-Grosse, Anne Mari Rokstad, Syed Ali, John D Lambris, Tom E Mollnes, Asbjørn M Nilsen, Jørgen Stenvik
Iron oxide nanoparticles (IONPs) are promising nanomaterials for biomedical applications. However, their inflammatory potential has not been fully established. Here, we used a lepirudin anti-coagulated human whole blood model to evaluate the potential of 10 nm IONPs to activate the complement system and induce cytokine production. Reactive oxygen species and cell death were also assessed. The IONPs activated complement, as measured by C3a, C5a and sC5b-9, and induced the production of pro-inflammatory cytokines in a particle-dose dependent manner, with the strongest response at 10 µg/mL IONPs...
2017: International Journal of Nanomedicine
https://www.readbyqxmd.com/read/28577241/human-infectious-diseases-and-risk-of-preeclampsia-an-updated-review-of-the-literature
#13
REVIEW
Malihe Nourollahpour Shiadeh, Zahra Behboodi Moghadam, Ishag Adam, Vafa Saber, Maryam Bagheri, Ali Rostami
BACKGROUND: Preeclampsia (PE) is one of the major causes of maternal and perinatal morbidity and mortality, especially in low- and middle-income countries. In recent years, a growing body of literatures suggests that infections by bacteria, viruses, and parasites and their related inflammations play an important role in the pathogenesis of PE. METHODS: We searched PubMed, Google scholar, and Cochrane databases using the following search words: "infection and preeclampsia," "bacterial infection and preeclampsia," "viral infection and preeclampsia" and "parasitic infection and preeclampsia...
June 2, 2017: Infection
https://www.readbyqxmd.com/read/28577176/complement-c5a-induces-mesenchymal-stem-cell-apoptosis-during-the-progression-of-chronic-diabetic-complications
#14
Ming Zhu, Xiao He, Xiao-Hui Wang, Wei Qiu, Wei Xing, Wei Guo, Tian-Chen An, Luo-Quan Ao, Xue-Ting Hu, Zhan Li, Xiao-Ping Liu, Nan Xiao, Jian Yu, Hong Huang, Xiang Xu
AIMS/HYPOTHESIS: Regeneration and repair mediated by mesenchymal stem cells (MSCs) are key self-protection mechanisms against diabetic complications, a reflection of diabetes-related cell/tissue damage and dysfunction. MSC abnormalities have been reported during the progression of diabetic complications, but little is known about whether a deficiency in these cells plays a role in the pathogenesis of this disease. In addition to MSC resident sites, peripheral circulation is a major source of MSCs that participate in the regeneration and repair of damaged tissue...
June 3, 2017: Diabetologia
https://www.readbyqxmd.com/read/28576324/new-concepts-on-the-therapeutic-control-of-complement-anaphylatoxin-receptors
#15
Owen A Hawksworth, Xaria X Li, Liam G Coulthard, Ernst J Wolvetang, Trent M Woodruff
The complement system is a pivotal driver of innate immunity, coordinating the host response to protect against pathogens. At the heart of the complement response lie the active fragments, C3a and C5a, acting through their specific receptors, C3aR, C5aR1, and C5aR2, to direct the cellular response to inflammation. Their potent function however, places them at risk of damaging the host, with aberrant C3a and C5a signaling activity linked to a wide range of disorders of inflammatory, autoimmune, and neurodegenerative etiologies...
May 30, 2017: Molecular Immunology
https://www.readbyqxmd.com/read/28572445/complement-induced-activation-of-mapks-and-akt-during-sepsis-role-in-cardiac-dysfunction
#16
Fatemeh Fattahi, Miriam Kalbitz, Elizabeth A Malan, Elizabeth Abe, Lawrence Jajou, Markus S Huber-Lang, Markus Bosmann, Mark W Russell, Firas S Zetoune, Peter A Ward
Polymicrobial sepsis in mice causes myocardial dysfunction after generation of the complement anaphylatoxin, complement component 5a (C5a). C5a interacts with its receptors on cardiomyocytes (CMs), resulting in redox imbalance and cardiac dysfunction that can be functionally measured and quantitated using echocardiology/Doppler technology. In this report we have evaluated activation of MAPKs and Akt in CMs exposed to C5a in vitro and after cecal ligation and puncture (CLP) in vivo In both cases, C5a in vitro caused activation (phosphorylation) of MAPKs and Akt in CMs, which required availability of both C5a receptors...
June 1, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28571586/complement-c5a-c5ar1-signalling-drives-skeletal-muscle-macrophage-recruitment-in-the-hsod1-g93a-mouse-model-of-amyotrophic-lateral-sclerosis
#17
Haitao A Wang, John D Lee, Kah Meng Lee, Trent M Woodruff, Peter G Noakes
BACKGROUND: The terminal pathway of the innate immune complement system is implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). Terminal complement activation leads to generation of C5a, which through its receptor, C5aR1, drives immune cell recruitment and activation. Importantly, genetic or pharmacological blockage of C5aR1 improves motor performance and reduces disease pathology in hSOD1(G93A) rodent models of ALS. In this study, we aimed to explore the potential mechanisms of C5aR1-mediated pathology in hSOD1(G93A) mice by examining their skeletal muscles...
June 1, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28567671/downregulation-of-the-complement-cascade-in-vitro-in-mice-and-in-patients-with-cardiovascular-disease-by-the-bet-protein-inhibitor-apabetalone-rvx-208
#18
Sylwia Wasiak, Dean Gilham, Laura M Tsujikawa, Christopher Halliday, Cyrus Calosing, Ravi Jahagirdar, Jan Johansson, Michael Sweeney, Norman C Wong, Ewelina Kulikowski
Apabetalone (RVX-208) is an epigenetic regulator developed to treat cardiovascular disease (CVD) that targets BET proteins. Through transcriptional regulation RVX-208 modulates pathways that underlie CVD including reverse cholesterol transport, vascular inflammation, coagulation, and complement. Using transcriptomics and proteomics we show that complement is one of the top pathways downregulated by RVX-208 in primary human hepatocytes (PHH) and in plasma from CVD patients. RVX-208 reduces basal and cytokine-driven expression of complement factors in PHH and in chimeric mice with humanized livers...
May 31, 2017: Journal of Cardiovascular Translational Research
https://www.readbyqxmd.com/read/28559893/upregulation-of-early-and-downregulation-of-terminal-pathway-complement-genes-in-subcutaneous-adipose-tissue-and-adipocytes-in-acquired-obesity
#19
Sanna Kaye, A Inkeri Lokki, Anna Hanttu, Eija Nissilä, Sini Heinonen, Antti Hakkarainen, Jesper Lundbom, Nina Lundbom, Lilli Saarinen, Olli Tynninen, Maheswary Muniandy, Aila Rissanen, Jaakko Kaprio, Seppo Meri, Kirsi H Pietiläinen
Inflammation is an important mediator of obesity-related complications such as the metabolic syndrome but its causes and mechanisms are unknown. As the complement system is a key mediator of inflammation, we studied whether it is activated in acquired obesity in subcutaneous adipose tissue (AT) and isolated adipocytes. We used a special study design of genetically matched controls of lean and heavy groups, rare monozygotic twin pairs discordant for body mass index (BMI) [n = 26, within-pair difference (Δ) in body mass index, BMI >3 kg/m(2)] with as much as 18 kg mean Δweight...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28539873/pharmacological-stimulation-of-phagocytosis-enhances-amyloid-plaque-clearance-evidence-from-a-transgenic-mouse-model-of-attr-neuropathy
#20
Eleni Fella, Kleitos Sokratous, Revekka Papacharalambous, Kyriacos Kyriacou, Joy Phillips, Sam Sanderson, Elena Panayiotou, Theodoros Kyriakides
Hereditary ATTR V30M amyloidosis is a lethal autosomal dominant sensorimotor and autonomic neuropathy caused by deposition of aberrant transthyretin (TTR). Immunohistochemical examination of sural nerve biopsies in patients with amyloidotic neuropathy show co-aggregation of TTR with several proteins; including apolipoprotein E, serum amyloid P and components of the complement cascade. Complement activation and macrophages are increasingly recognized to play a crucial role in amyloidogenesis at the tissue bed level...
2017: Frontiers in Molecular Neuroscience
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