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https://www.readbyqxmd.com/read/28332617/molecular-epidemiology-of-acute-hemorrhagic-conjunctivitis-caused-by-coxsackie-a-type-24-variant-in-china-2004-2014
#1
Li Zhang, Na Zhao, Xiaodan Huang, Xiuming Jin, Xingyi Geng, Ta-Chien Chan, Shelan Liu
To understand control interventions, the molecular epidemiology of acute hemorrhagic conjunctivitis (AHC) was investigated from 2004 to 2014.A total of 613,485 AHC cases (annualized cases 55,771) with two deaths were included. Our findings showed that AHC was reported in all provinces, predominantly in Southern and Eastern China. The incidence rates were highest in 2007 (5.65/100,000) and 2010 (21.78/100,000) respectively. A clear seasonal pattern was identified with a peak from August to October. AHC cases occurred in all age groups; however, five to 14 years was the predominant group [23...
March 23, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28326060/microbial-neuraminidase-induces-a-moderate-and-transient-myelin-vacuolation-independent-of-complement-system-activation
#2
Pablo Granados-Durán, María Dolores López-Ávalos, Manuel Cifuentes, Margarita Pérez-Martín, María Del Mar Fernández-Arjona, Timothy R Hughes, Krista Johnson, B Paul Morgan, Pedro Fernández-Llebrez, Jesús M Grondona
AIMS: Some central nervous system pathogens express neuraminidase (NA) on their surfaces. In the rat brain, a single intracerebroventricular (ICV) injection of NA induces myelin vacuolation in axonal tracts. Here, we explore the nature, the time course, and the role of the complement system in this damage. METHODS: The spatiotemporal analysis of myelin vacuolation was performed by optical and electron microscopy. Myelin basic protein-positive area and oligodendrocyte transcription factor (Olig2)-positive cells were quantified in the damaged bundles...
2017: Frontiers in Neurology
https://www.readbyqxmd.com/read/28323848/7%C3%AE-hydroxycholesterol-induces-monocyte-macrophage-cell-expression-of-interleukin-8-via-c5a-receptor
#3
Hyok-Rae Cho, Yonghae Son, Sun-Mi Kim, Bo-Young Kim, Seong-Kug Eo, Young Chul Park, Koanhoi Kim
We investigated effects of 7-oxygenated cholesterol derivatives present in atherosclerotic lesions, 7α-hydroxycholesterol (7αOHChol), 7β-hydroxycholesterol (7βOHChol), and 7-ketocholesterol (7K), on IL-8 expression. Transcript levels of IL-8 and secretion of its corresponding gene product by monocytes/macrophages were enhanced by treatment with 7αOHChol and, to a lesser extent, 7K, but not by 7βOHChol. The 7-oxygenated cholesterol derivatives, however, did not change transcription of the IL-8 gene in vascular smooth muscle cells...
2017: PloS One
https://www.readbyqxmd.com/read/28316335/complement-in-anca-associated-vasculitis-mechanisms-and-implications-for-management
#4
REVIEW
Min Chen, David R W Jayne, Ming-Hui Zhao
Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a group of potentially life-threatening autoimmune diseases. The main histological feature in the kidneys of patients with AAV is pauci-immune necrotizing crescentic glomerulonephritis with little immunoglobulin and complement deposition in the glomerular capillary walls. The complement system was not, therefore, initially thought to be associated with the development of AAV. Accumulating evidence from animal models and clinical observations indicate, however, that activation of the complement system - and the alternative pathway in particular - is crucial for the development of AAV, and that the complement activation product C5a has a central role...
March 20, 2017: Nature Reviews. Nephrology
https://www.readbyqxmd.com/read/28315675/low-intensity-training-and-the-c5a-complement-antagonist-nox-d21-rescue-the-mdx-phenotype-through-modulation-of-inflammation
#5
Janek Hyzewicz, Jun Tanihata, Mutsuki Kuraoka, Yuko Nitahara-Kasahara, Teiva Beylier, Urs T Ruegg, Axel Vater, Shin'ichi Takeda
Inflammatory events occurring in dystrophic muscles contribute to the progression of Duchenne muscular dystrophy (DMD). Low-intensity training (LIT) attenuates the phenotype of mdx mice, an animal model for DMD. Therefore, we postulated that LIT could have anti-inflammatory properties. We assessed levels of inflammatory cytokines and infiltrated immune cells in gastrocnemius muscle of mdx mice after LIT. We detected high levels of complement component C5a, chemokine ligand (CCL) 2, CD68(+) monocytes/macrophages, and proinflammatory M1 macrophages in muscles of mdx mice...
March 15, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28301559/synergy-between-the-classical-and-alternative-pathways-of-complement-is-essential-for-conferring-effective-protection-against-the-pandemic-influenza-a-h1n1-2009-virus-infection
#6
Ajitanuj Rattan, Shailesh D Pawar, Renuka Nawadkar, Neeraja Kulkarni, Girdhari Lal, Jayati Mullick, Arvind Sahu
The pandemic influenza A(H1N1) 2009 virus caused significant morbidity and mortality worldwide thus necessitating the need to understand the host factors that influence its control. Previously, the complement system has been shown to provide protection during the seasonal influenza virus infection, however, the role of individual complement pathways is not yet clear. Here, we have dissected the role of intact complement as well as of its individual activation pathways during the pandemic influenza virus infection using mouse strains deficient in various complement components...
March 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28295247/targeting-c3a-c5a-receptors-inhibits-human-mesangial-cell-proliferation-and-alleviates-iga-nephropathy-in-mice
#7
Ying Zhang, Xianli Yan, Ting Zhao, Qihe Xu, Qi Peng, Ruimin Hu, Songxia Quan, Yali Zhou, Guolan Xing
Complement activation has a deep pathogenic influence in IgA nephropathy (IgAN). C3a and C5a, small cleavage fragments generated by complement activation, are key mediators of inflammation. The fragments exert broad pro-inflammatory effects by binding to specific receptors (C3aR and C5aR, respectively). However, no studies thus far have investigated the effects of C3a, C5a and their receptors on IgAN. We observed that C3aR and C5aR antagonists repressed IgA-induced cell proliferation and IL-6 and MCP-1 production in cultured human mesangial cells (HMCs)...
March 15, 2017: Clinical and Experimental Immunology
https://www.readbyqxmd.com/read/28288993/a-combined-pd-1-c5a-blockade-synergistically-protects-against-lung-cancer-growth-and-metastasis
#8
Daniel Ajona, Sergio Ortiz-Espinosa, Haritz Moreno, Teresa Lozano, Maria J Pajares, Jackeline Agorreta, Cristina Bértolo, Juan J Lasarte, Silvestre Vicent, Axel Vater, Fernando Lecanda, Luis M Montuenga, Ruben Pio
Disruption of the programmed cell death protein 1 (PD-1) pathway with immune checkpoint inhibitors represents a major breakthrough in the treatment of non-small cell lung cancer. We hypothesized that a combined inhibition of C5a/C5aR1 and PD-1 signaling may have an antitumor synergistic effect. RMP1-14 antibody was used to block PD-1 and an L-aptamer to inhibit signaling of complement C5a with its receptors. Using syngeneic models of lung cancer we demonstrate that the combination of C5a and PD-1 blockade markedly reduces tumor growth and metastasis, and leads to prolonged survival...
March 13, 2017: Cancer Discovery
https://www.readbyqxmd.com/read/28278205/complement-effectors-c5a-and-c3a-in-cystic-fibrosis-lung-fluid-correlate-with-disease-severity
#9
Pamela S Hair, Laura A Sass, Turaj Vazifedan, Tushar A Shah, Neel K Krishna, Kenji M Cunnion
In cystic fibrosis (CF), lung damage is mediated by a cycle of obstruction, infection, inflammation and tissue destruction. The complement system is a major mediator of inflammation for many diseases with the effectors C5a and C3a often playing important roles. We have previously shown in a small pilot study that CF sputum soluble fraction concentrations of C5a and C3a were associated with clinical measures of CF disease. Here we report a much larger study of 34 CF subjects providing 169 testable sputum samples allowing longitudinal evaluation comparing C5a and C3a with clinical markers...
2017: PloS One
https://www.readbyqxmd.com/read/28275134/the-complement-anaphylatoxins-c5a-and-c3a-suppress-ifn-%C3%AE-production-in-response-to-listeria-monocytogenes-by-inhibition-of-the-cyclic-dinucleotide-activated-cytosolic-surveillance-pathway
#10
Stacey L Mueller-Ortiz, Daniel G Calame, Nancy Shenoi, Yi-Dong Li, Rick A Wetsel
Listeria monocytogenes is an intracellular Gram-positive bacterium that induces expression of type I IFNs (IFN-α/IFN-β) during infection. These cytokines are detrimental to the host during infection by priming leukocytes to undergo L. monocytogenes-mediated apoptosis. Our previous studies showed that C5aR1(-/-) and C3aR(-/-) mice are highly susceptible to L. monocytogenes infection as a result of increased IFN-β-mediated apoptosis of major leukocyte cell populations, including CD4(+) and CD8(+) T cells. However, the mechanisms by which C3a and C5a modulate IFN-β expression during L...
March 8, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28262211/complement-alternative-pathway-s-activation-in-patients-with-lupus-nephritis
#11
Di Song, Wei-Yi Guo, Feng-Mei Wang, Yong-Zhe Li, Yan Song, Feng Yu, Ming-Hui Zhao
OBJECTIVE: The aim of this study was to detect the spectrum of complement activation pathways in circulation and to assess their correlations with clinical and pathologic features in a large lupus nephritis cohort from China. MATERIALS AND METHODS: Plasma levels of C1q, mannose-binding lectin, C4d, Bb, C3, C3a, C5a and soluble C5b-9 were detected by enzyme-linked immunosorbent assay in 222 patients with active biopsy-proven lupus nephritis, 34 patients with lupus nephritis at remission, 82 patients with active systemic lupus erythematosus without renal involvement and 39 normal controls...
March 2017: American Journal of the Medical Sciences
https://www.readbyqxmd.com/read/28248200/the-role-of-the-complement-system-in-cancer
#12
REVIEW
Vahid Afshar-Kharghan
In addition to being a component of innate immunity and an ancient defense mechanism against invading pathogens, complement activation also participates in the adaptive immune response, inflammation, hemostasis, embryogenesis, and organ repair and development. Activation of the complement system via classical, lectin, or alternative pathways generates anaphylatoxins (C3a and C5a) and membrane attack complex (C5b-9) and opsonizes targeted cells. Complement activation end products and their receptors mediate cell-cell interactions that regulate several biological functions in the extravascular tissue...
March 1, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28237029/c5ar-contributes-to-the-weak-th1-profile-induced-by-an-outbreak-strain-of-mycobacterium-tuberculosis
#13
Carmen Alejandra Sabio Y García, Noemí Yokobori, Juan Ignacio Basile, Luciana Balboa, Alejandra González, Beatriz López, Viviana Ritacco, Silvia de la Barrera, María Del Carmen Sasiain
C5a anaphylatoxin is a component of the complement system involved in the modulation of T-cell polarization. Herein we investigated whether C5a receptors, C5aR and C5L2, modulate the cytokine profiles induced by Mycobacterium tuberculosis (Mtb). We analyzed the impact of both receptors on T helper cell polarization induced by the multidrug resistant outbreak strain named M, which is a poor IFN-γ inducer compared with the laboratory strain H37Rv. To this aim, we first blocked C5aR or C5L2 of peripheral blood monocytes (Mo) from patients with tuberculosis and healthy donors, then we stimulated the Mo either with H37Rv or the M strain, and finally we analyzed cytokine profiles of Mo/macrophages (MΦ) and CD4(+) T-cells...
March 2017: Tuberculosis
https://www.readbyqxmd.com/read/28231307/differential-regulation-of-c5a-receptor-1-in-innate-immune-cells-during-the-allergic-asthma-effector-phase
#14
Fanny Ender, Anna V Wiese, Inken Schmudde, Jing Sun, Tillman Vollbrandt, Peter König, Yves Laumonnier, Jörg Köhl
C5a drives airway constriction and inflammation during the effector phase of allergic asthma, mainly through the activation of C5a receptor 1 (C5aR1). Yet, C5aR1 expression on myeloid and lymphoid cells during the allergic effector phase is ill-defined. Recently, we generated and characterized a floxed green fluorescent protein (GFP)-C5aR1 knock-in mouse. Here, we used this reporter strain to monitor C5aR1 expression in airway, pulmonary and lymph node cells during the effector phase of OVA-driven allergic asthma...
2017: PloS One
https://www.readbyqxmd.com/read/28228558/the-ribosomal-protein-s19-suppresses-antitumor-immune-responses-via-the-complement-c5a-receptor-1
#15
Maciej M Markiewski, Surya Kumari Vadrevu, Sharad K Sharma, Navin Kumar Chintala, Shanawaz Ghouse, Jun-Hung Cho, David P Fairlie, Yvonne Paterson, Aristotelis Astrinidis, Magdalena Karbowniczek
Relatively little is known about factors that initiate immunosuppression in tumors and act at the interface between tumor cells and host cells. In this article, we report novel immunosuppressive properties of the ribosomal protein S19 (RPS19), which is upregulated in human breast and ovarian cancer cells and released from apoptotic tumor cells, whereupon it interacts with the complement C5a receptor 1 expressed on tumor infiltrating myeloid-derived suppressor cells. This interaction promotes tumor growth by facilitating recruitment of these cells to tumors...
April 1, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28225753/complement-drives-glucosylceramide-accumulation-and-tissue-inflammation-in-gaucher-disease
#16
Manoj K Pandey, Thomas A Burrow, Reena Rani, Lisa J Martin, David Witte, Kenneth D Setchell, Mary A Mckay, Albert F Magnusen, Wujuan Zhang, Benjamin Liou, Jörg Köhl, Gregory A Grabowski
Gaucher disease is caused by mutations in GBA1, which encodes the lysosomal enzyme glucocerebrosidase (GCase). GBA1 mutations drive extensive accumulation of glucosylceramide (GC) in multiple innate and adaptive immune cells in the spleen, liver, lung and bone marrow, often leading to chronic inflammation. The mechanisms that connect excess GC to tissue inflammation remain unknown. Here we show that activation of complement C5a and C5a receptor 1 (C5aR1) controls GC accumulation and the inflammatory response in experimental and clinical Gaucher disease...
February 22, 2017: Nature
https://www.readbyqxmd.com/read/28190533/the-roles-of-a-ribosomal-protein-s19-polymer-in-a-mouse-model-of-carrageenan-induced-acute-pleurisy
#17
Koji Yamanegi, Toru Kawakami, Naoko Yamada, Shunsuke Kumanishi, Hiroyuki Futani, Keiji Nakasho, Hiroshi Nishiura
C5-deficient mice usually present moderate neutrophil activation during the initiation phase of acute inflammation. Conversely, C5a receptor (C5aR)-deficient mice show unusually excessive activation of neutrophils. We identified the ribosomal protein S19 (RP S19) polymer, which is cross-linked at Lys122 and Gln137 by transglutaminases in apoptotic neutrophils, as a second C5aR ligand during the resolution phase of acute inflammation. The RP S19 polymer promotes apoptosis via the neutrophil C5aR and phagocytosis via the macrophage C5aR...
February 7, 2017: Immunobiology
https://www.readbyqxmd.com/read/28173736/the-alternative-receptor-for-complement-component-5a-c5ar2-conveys-neuroprotection-in-traumatic-spinal-cord-injury
#18
Patrick Biggins, Faith Brennan, Stephen Taylor, Trent Woodruff, Marc Ruitenberg
This study investigated the role of the secondary receptor for complement activation fragment C5a, C5aR2, in secondary inflammatory pathology following contusive spinal cord injury (SCI) in mice. <i>C5ar2<sup>-/-</sup></i> mice exhibited decreased intraparenchymal TNFα and IL-6 acutely after injury but these reductions did not translate into improved outcomes. We show that loss of C5aR2 leads to increased lesion volumes, reduced myelin sparing and significantly worsened recovery from SCI in <i>C5ar2<sup>-/-</sup></i> animals compared to wild-type (WT) controls...
February 7, 2017: Journal of Neurotrauma
https://www.readbyqxmd.com/read/28167912/c5a-regulates-il-1%C3%AE-production-and-leukocyte-recruitment-in-a-murine-model-of-monosodium-urate-crystal-induced-peritonitis
#19
Hanif J Khameneh, Adrian W S Ho, Federica Laudisi, Heidi Derks, Matheswaran Kandasamy, Baalasubramanian Sivasankar, Gim Gee Teng, Alessandra Mortellaro
Gouty arthritis results from the generation of monosodium urate (MSU) crystals within joints. These MSU crystals elicit acute inflammation characterized by massive infiltration of neutrophils and monocytes that are mobilized by the pro-inflammatory cytokine IL-1β. MSU crystals also activate the complement system, which regulates the inflammatory response; however, it is unclear whether or how MSU-mediated complement activation is linked to IL-1β release in vivo, and the various roles that might be played by individual components of the complement cascade...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28143910/paper-of-note-in-science-immunology-2-7
#20
John F Foley
This month's article shows how the complement C5a receptor initiates the recruitment of neutrophils into joint endothelium in a mouse model of arthritis.
January 31, 2017: Science Signaling
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