Relevant bibliographies by topics / Anaphylatoxin

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Anaphylatoxin'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Anaphylatoxin"

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Bautsch, W., T. Kretzschmar, T. Stühmer, A. Kola, M. Emde, J. Köhl, A. Klos, and D. Bitter-Suermann. "A recombinant hybrid anaphylatoxin with dual C3a/C5a activity." Biochemical Journal 288, no. 1 (November 15, 1992): 261–66. http://dx.doi.org/10.1042/bj2880261.

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By site-directed mutagenesis of a human complement factor C5a cDNA clone, we have designed a hybrid anaphylatoxin in which three amino acid residues in the C-terminal sequence of human C5a were exchanged to create the native C-terminal human C3a (hC3a) sequence Leu-Gly-Leu-Ala-Arg. This hybrid anaphylatoxin rC5a-(1-69)-LGLAR exhibited true C3a and C5a activity when tested in the guinea pig ileum contraction assay. Quantitative measurements of ATP release from guinea pig platelets revealed about 1% intrinsic C3a activity for this hybrid, while the C5a activity was essentially unchanged. Competitive binding assays confirmed that the rC5a-(1-69)-LGLAR mutant was able to displace radioiodinated rhC5a with a KI of approx. 40 nM and hC3a with a KI of approx. 3.7 microM from guinea pig platelets. Since the C-termini of both human C3a and C5a anaphylatoxins are known to interact with their respective receptors, we conclude that the same peptidic sequence, LGLAR, is able to bind to and activate two different receptors, the C3a receptor as well as the C5a receptor. This clone provides a novel tool for the identification of further receptor-binding residues in both anaphylatoxins, since any mutants may be tested for altered C3a and C5a activity simultaneously.
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Jekic, M., and Ivan Jekic. "172 ANAPHYLATOXIN." Shock 3, no. 5 (May 1995): 53. http://dx.doi.org/10.1097/00024382-199505000-00173.

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Bengtson, Anders. "Anaphylatoxin Formation in Sepsis." Archives of Surgery 123, no. 5 (May 1, 1988): 645. http://dx.doi.org/10.1001/archsurg.1988.01400290131023.

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Hartmann, Karin, Beate M. Henz, Sabine Krüger-Krasagakes, Jörg Köhl, Reinhard Burger, Sven Guhl, Ingo Haase, Undine Lippert, and Torsten Zuberbier. "C3a and C5a Stimulate Chemotaxis of Human Mast Cells." Blood 89, no. 8 (April 15, 1997): 2863–70. http://dx.doi.org/10.1182/blood.v89.8.2863.

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Abstract The factors that control migration of mast cells to sites of inflammation and tissue repair remain largely undefined. Whereas several recent studies have described chemotactic factors that induce migration of murine mast cells, only stem cell factor (SCF ) is known to induce migration of human mast cells. We report here that the anaphylatoxins C3a and C5a are chemotactic factors for the human mast cell line HMC-1, human cord blood-derived mast cells (CBMC) and cutaneous mast cells in vitro. The presence of an extracellular matrix protein, laminin, was required for chemotaxis in response to complement peptides. Migration of mast cells towards C3a and C5a was dose-dependent, peaking at 1 μg/mL (100 nmol/L), and was inhibited by specific antibodies. Pretreatment with pertussis toxin inhibited the anaphylatoxin-mediated migration of HMC-1 cells, indicating that Gi proteins are involved in complement-activated signal transduction pathways in human mast cells. Both C3a and C5a also induced a rapid and transient mobilization of intracellular free calcium ([Ca2+]i ) in HMC-1 cells. Besides SCF, other chemotactic factors tested, such as interleukin-3, nerve growth factor, transforming growth factor β, RANTES (regulated upon activation, normal T cell expressed and secreted), monocyte chemotactic protein-1 (MCP-1), MCP-2, MCP-3, macrophage inflammatory protein-1α (MIP-1α), and MIP-1β, failed to stimulate migration of human mast cells. In summary, these findings indicate that C3a and C5a serve as chemotaxins for human mast cells. Anaphylatoxin-mediated recruitment of mast cells might play an important role in hypersensitivity and inflammatory processes.
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Chenoweth, Dennis E. "Anaphylatoxin Formation in Extracorporeal Circuits." Complement 3, no. 3 (1986): 152–65. http://dx.doi.org/10.1159/000467892.

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Ibrahim, Farazeela Bte Mohd, See Jay Pang, and Alirio J. Melendez. "Anaphylatoxin Signaling in Human Neutrophils." Journal of Biological Chemistry 279, no. 43 (August 9, 2004): 44802–11. http://dx.doi.org/10.1074/jbc.m403977200.

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Taylor, Stephen M., and David P. Fairlie. "Regulators of the anaphylatoxin C5a." Expert Opinion on Therapeutic Patents 10, no. 4 (April 2000): 449–58. http://dx.doi.org/10.1517/13543776.10.4.449.

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Roxvall, Lennart, Anders Bengtson, and Mats Heideman. "Anaphylatoxin generation in acute pancreatitis." Journal of Surgical Research 47, no. 2 (August 1989): 138–43. http://dx.doi.org/10.1016/0022-4804(89)90078-4.

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Tanabe, Ithallo S. B., Elane C. Santos, Eloiza L. L. Tanabe, Stephannie J. M. Souza, Fabio E. F. Santos, Jamile Taniele-Silva, Jean F. G. Ferro, et al. "Cytokines and chemokines triggered by Chikungunya virus infection in human patients during the very early acute phase." Transactions of The Royal Society of Tropical Medicine and Hygiene 113, no. 11 (July 31, 2019): 730–33. http://dx.doi.org/10.1093/trstmh/trz065.

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Abstract Background The immune response against the Chikungunya virus (CHIKV) during the very early acute phase is not fully elucidated. Therefore we explored the cytokine and chemokine profile triggered by CHIKV in infected patients. Methods Cytokines, chemokines and C5a anaphylatoxin were analysed in serum from CHIKV-infected patients during the viraemic phase (mean 2.97±1.27 d after illness onset) compared with a healthy group. Results CHIKV-infected patients had a significant increase of interferon-α (IFN-α), interleukin-6 (IL-6), interleukin-8 (CXCL8/IL-8), interleukin-10 (IL-10), interferon-γ (IFN-γ), monokine induced by interferon-γ (CXCL9/MIG), monocyte chemoattractant protein-1 (CCL2/MCP-1), interferon-γ-induced protein-10 (CXCL10/IP-10) and complement C5a anaphylatoxin. Conclusions The very early acute immune response triggered against CHIKV leads to an increase in pro-inflammatory immune mediators such as IFN-γ and its induced chemokines, and a high level of C5a anaphylatoxin as a result of complement activation.
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Bestebroer, Jovanka, Kok P. M. van Kessel, Hafida Azouagh, Annemiek M. Walenkamp, Ingrid G. J. Boer, Roland A. Romijn, Jos A. G. van Strijp, and Carla J. C. de Haas. "Staphylococcal SSL5 inhibits leukocyte activation by chemokines and anaphylatoxins." Blood 113, no. 2 (January 8, 2009): 328–37. http://dx.doi.org/10.1182/blood-2008-04-153882.

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Abstract Staphylococcus aureus secretes several virulence factors modulating immune responses. Staphylococcal superantigen-like (SSL) proteins are a family of 14 exotoxins with homology to superantigens, but with generally unknown function. Recently, we showed that SSL5 binds to P-selectin glycoprotein ligand 1 dependently of sialyl Lewis X and inhibits P-selectin–dependent neutrophil rolling. Here, we show that SSL5 potently and specifically inhibits leukocyte activation by anaphylatoxins and all classes of chemokines. SSL5 inhibited calcium mobilization, actin polymerization, and chemotaxis induced by chemokines and anaphylatoxins but not by other chemoattractants. Antibody competition experiments showed that SSL5 targets several chemokine and anaphylatoxin receptors. In addition, transfection studies showed that SSL5 binds glycosylated N-termini of all G protein–coupled receptors (GPCRs) but only inhibits stimuli of protein nature that require the receptor N-terminus for activation. Furthermore, SSL5 increased binding of chemokines to cells independent of chemokine receptors through their common glycosaminoglycan-binding site. Importance of glycans was shown for both GPCR and chemokine binding. Thus, SSL5 is an important immunomodulatory protein of S aureus that targets several crucial, initial stages of leukocyte extravasation. It is therefore a potential new antiinflammatory compound for diseases associated with chemoattractants and their receptors and disorders characterized by excessive recruitment of leukocytes.
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Dissertations / Theses on the topic "Anaphylatoxin"

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Symon, Fiona A. "A receptor for human anaphylatoxin C3a on HL60 cells." Thesis, University of Aberdeen, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334087.

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The anaphylatoxin, C3a, generated from C3 during complement activation, exhibits a wide range of biological activities which suggest it is a potent inflammatory and immunoregulatory mediator. These actions are thought to be mediated via specific cell surface receptors; however, only guinea pig platelets have been shown, conclusively, to express receptors recognising C3a. The objective of this project was to identify a human cell type expressing C3a receptors and to characterise that receptor. In order to characterise the human C3a receptor, relatively large quantities of human C3a had to be purified. Initially, C3a was prepared from a tryptic digest of C3, which had been isolated from human plasma. However, a heterogeneous mixture of predominantly inactive C3a-like polypeptides was obtained. Latterly, C3a was prepared directly from complement-activated serum, which provided a pure sample of intact protein. C3a produced by this second method was radio-iodinated and used to characterise the C3a receptor on the human promyelocytic cell line, HL60. Characterisation of the receptors on the differentiated cell line indicated that 125l-C3a binding was rapid and temperature dependent, apparently resulting in ligand-receptor complex internalisation and intracellular processing. This binding was shown to be saturable and specific for C3a as the inactive C3a-des-Arg was not recognised by the receptor. Together, this evidence pointed to the presence of a specific C3a receptor expressed on differentiated HL60 cells and estimated by Scatchard analysis to be present at 65000-74000 sites/cell with a Kd of 0.71-1.0 x 10-9 M. Estimates of the molecular size of the HL60 C3a receptor, by SDS/PAGE, indicated that C3a forms a 119-132 kDa complex when cross-linked to differentiated HL60 cells. Subtraction of the molecular weight of C3a indicated a size of 110-132 kDa for the receptor protein. Radio-ligand blotting experiments showed C3a to associate with two HL60 membrane proteins of molecular weights of 79-80 and 83-85 kDa. The difference in mass between cross-linked and ligand-blotted species may be due to association with a GTP-binding protein subunit in the cross-linking experiments.
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Zhang, Xun. "Immunoregulatory Roles of the Anaphylatoxin Receptors in Experimental Allergic Asthma." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1250600916.

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Silawal, Sandeep [Verfasser]. "Komplementregulation in Sehnenzellen, vermittelt durch das Anaphylatoxin C5a und Leukozyten / Sandeep Silawal." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1148425276/34.

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MacKinnon, Johan. "Human anaphylatoxin C3a : assay and recombinant fusion protein expression in Saccharomyces cerevisiae." Thesis, University of Aberdeen, 1991. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU033675.

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Native human C3a has been purified from plasma in an active form, setting up what is now a routine purification procedure in this laboratory. An assay system has been selected from a range of methods for measuring the activity of C3s. This method measures the release of histamine from human peripheral blood basophils in response to the interaction between C3a and the cell surface receptor. The quantitation of histamine release is based on the condensation of histamine with orthophthalaldehyde to form a fluorescent product with three stereoisomers, which can be separated and quantified using HPLC with fluorescence detection. The coding sequence for human anaphylatoxin C3a has been cloned into the PGK structural gene of the yeast/E. coli shuttle vector pMA27 to create the coding sequence for a PGK-C3a fusion protein. The DNA code for the recognition and target sequence for the proteolytic enzyme blood coagulation factor Xa (lle-Glu-Arg) was also introduced, using oligonucleotide-directed mutagenesis, between the PGK and C3a codes, to enable in vitro cleavage of the proteins to be carried out subsequent to expression in a suitable microbial host. The Saccharomyces cerevisiae host strain MT302/28b has been transformed with the plasmid encoding the fusion product and expression of the desired protein detected.
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Püschel, Gerhard P., Ursula Hespeling, Martin Oppermann, and Peter Dieter. "Increase in prostanoid formation in rat liver macrophages (Kupffer cells) by human anaphylatoxin C3a." Universität Potsdam, 1993. http://opus.kobv.de/ubp/volltexte/2008/1671/.

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Human anaphylatoxin C3a increases glycogenolysis in perfused rat liver. This action is inhibited by prostanoid synthesis inhibitors and prostanoid antagonists. Because prostanoids but not anaphylatoxin C3a can increase glycogenolysis in hepatocytes, it has been proposed that prostanoid formation in nonparenchymal cells represents an important step in the C3a-dependent increase in hepatic glycogenolysis. This study shows that (a) human anaphylatoxin C3a (0.1 to 10 mug/ml) dose-dependently increased prostaglandin D2, thromboxane B, and prostaglandin F2alpha formation in rat liver macrophages (Kupffer cells); (b) the C3a-mediated increase in prostanoid formation was maximal after 2 min and showed tachyphylaxis; and (c) the C3a-elicited prostanoid formation could be inhibited specifically by preincubation of C3a with carboxypeptidase B to remove the essential C-terminal arginine or by preincubation of C3a with Fab fragments of a neutralizing monoclonal antibody. These data support the hypothesis that the C3a-dependent activation of hepatic glycogenolysis is mediated by way of a C3a-induced prostanoid production in Kupffer cells.
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Schaefer, Myriam. "Analyse der transkriptionellen Regulation des C3a-Rezeptors & der Genexpression monozytärer Zellen nach Anaphylatoxin-Stimulation." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=974105155.

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Cossham, Michael Leonard Kenyon [Verfasser]. "Optimierung der Komplementaktivierung eines EGFR-Antikörpers führt zu verstärkter Aktivierung von Granulozyten mittels Anaphylatoxin C5a / Michael Leonard Kenyon Cossham." Kiel : Universitätsbibliothek Kiel, 2017. http://d-nb.info/1131075951/34.

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Wood, Alexander James Telfer. "Measurement and mechanisms of complement-induced neutrophil dysfunction." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/289984.

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Critical illness is an aetiologically and clinically heterogeneous syndrome that is characterised by organ failure and immune dysfunction. Mortality in critically ill patients is driven by inflammation-associated organ damage and a profound vulnerability to nosocomial infection. Both factors are influenced by the complement protein C5a, released by unbridled activation of the complement system during critical illness. C5a suppresses antimicrobial functions of key immune cells, in particular the neutrophil, and this suppression has been shown to be associated with poorer outcomes amongst critically ill adults. The intracellular signalling pathways which mediate C5a-induced neutrophil dysfunction are incompletely understood, and scalable tools with which to assess immune cell dysfunction in patients are lacking. This thesis aimed to develop tools with which to assess neutrophil function and delineate intracellular signalling pathways driving C5a-induced impairment. Neutrophils were isolated from healthy volunteer blood and functions (priming, phagocytosis and reactive oxygen species production) were assessed using light microscopy, confocal microscopy and flow cytometry. A new assay was developed using an Attune Nxt™ acoustic focusing cytometer (Life Technologies) which allowed the rapid assessment of multiple neutrophil functions in small samples of unlysed, minimally-manipulated human whole blood. Complete proteomes and phosphoproteomes of phagocytosing neutrophils were obtained from four healthy donors pre-treated with C5a or vehicle control. Several key insights were gained from this work and are summarised here. Firstly, C5a was found to induce a prolonged (greater than seven hours) impairment of neutrophil phagocytosis. This defect was found to be preventable by previous or concurrent phagocytosis, indicating common signalling mechanisms. Secondly, a novel assay was developed which allows the rapid assessment of multiple neutrophil functions in less than 2 mL of whole blood, and this assay can feasibly be applied in clinical settings. Thirdly, cell-surface expression of the C5a receptor was found to be markedly decreased during phagocytosis, and this decrease was not mediated by protease activity. Finally, unbiased proteomics quantified 4859 proteins and 2712 phosphoproteins respectively. This quantification is the deepest profile of the human neutrophil proteome published to date, and has revealed novel insights into the mechanisms of C5a-induced neutrophil dysfunction and phagocytosis.
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Püschel, Gerhard P., Martin Oppermann, Waldemar Muschol, Otto Götze, and Kurt Jungermann. "Increase of glucose and lactate output and decrease of flow by human anaphylatoxin C3a but not C5a in perfused rat liver." Universität Potsdam, 1989. http://opus.kobv.de/ubp/volltexte/2008/1673/.

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The complement fragments C3a and C5a were purified from zymosan-activated human serum by column chromatographic procedures after the bulk of the proteins had been removed by acidic polyethylene glycol precipitation. In the isolated in situ perfused rat liver C3a increased glucose and lactate output and reduced flow. Its effects were enhanced in the presence of the carboxypeptidase inhibitor DL-mercaptomethyl-3-guanidinoethylthio-propanoic acid (MERGETPA) and abolished by preincubation of the anaphylatoxin with carboxypeptidase B or with Fab fragments of an anti-C3a monoclonal antibody. The C3a effects were partially inhibited by the thromboxane antagonist BM13505. C5a had no effect. It is concluded that locally but not systemically produced C3a may play an important role in the regulation of local metabolism and hemodynamics during inflammatory processes in the liver.
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Holst, Benjamin. "Study of the capacity of Toll-like receptors to modulate pro-inflammatory responses mediated by receptors for the complement anaphylatoxin C5a." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/56693/.

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Toll-like receptors (TLRs) and the complement system play a crucial role in the innate immune response by mediating the initial recognition of, and prompt response to a variety of microorganisms. The concerted activation of TLRs and complement ensures efficient clearance of infection. Previous studies have documented synergism between TLRs and the receptor for the pro-inflammatory peptide C5a (C5aR/CD88), and regulation of TLR-induced pro-inflammatory responses by C5aR, suggesting crosstalk between TLRs and C5aR. However, it is unclear whether and how TLRs modulate C5a-induced pro-inflammatory responses. This study tested the hypothesis that a genuine, bi-directional signalling crosstalk between TLRs and C5a receptors exists, involving not only modulation of TLR-mediated responses by C5a receptor activation, but also modulation by TLR activation of the extent and/or quality of cellular responses to C5a. The experiments described in this thesis confirmed this hypothesis by demonstrating a marked positive modulatory effect of TLR activation on cell sensitivity to C5a in vitro and ex vivo and identifying underlying mechanistic targets. Pre-exposure of peripheral blood mononuclear cells and whole blood to diverse TLR ligands or bacteria enhanced C5a-induced pro-inflammatory responses. This effect was not observed in TLR4-signalling-deficient mice. TLR-induced hypersensitivity to C5a did not result from C5aR up-regulation or modulation of C5a-induced calcium mobilization. Rather, TLRs targeted the second C5a receptor, C5L2 (acting as a negative modulator of C5aR) by reducing C5L2 expression and activity. TLR-induced hypersensitivity to C5a was mimicked by blocking C5L2 and was not observed in C5L2KO mice. Furthermore, TLR activation inhibited C5L2 expression upon C5a stimulation. Expression of the key adaptor molecule β-arrestin 1, which mediates the inhibitory effects of C5L2 on C5aR, was also found to be negatively regulated by TLR activation. These findings identify a novel pathway of crosstalk within the innate immune system that amplifies innate host defence at the TLR-complement interface. Unravelling the mutually regulated activities of TLRs and complement may reveal new therapeutic avenues to control inflammation.
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Books on the topic "Anaphylatoxin"

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Hugli, Tony E. Immunobiology and Clinical Implications of the Complement Anaphylatoxins: Journal: Complement, Vol. 3, 1986 (Immunobiology & Clinical Implications of the Complement Anap). S. Karger AG (Switzerland), 1986.

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Book chapters on the topic "Anaphylatoxin"

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Hugli, T. E. "Structure and Function of C3a Anaphylatoxin*." In Current Topics in Microbiology and Immunology, 181–208. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74977-3_10.

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Mathews, Kenneth P. "Deficiencies in Regulator Proteins: 4. Anaphylatoxin Inactivator." In Hereditary and Acquired Complement Deficiencies in Animals and Man, 344–51. Basel: KARGER, 1987. http://dx.doi.org/10.1159/000318559.

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Habermann, Jens K., U. J. Roblick, B. T. Luke, D. A. Prieto, W. J. J. Finlay, V. N. Podust, J. M. Roman, et al. "Serumtest für C3a Anaphylatoxin ermöglicht minimal-invasives Screening für kolorektale Tumoren." In Chirurgisches Forum 2008, 111–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-78833-1_41.

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Köhl, J., and D. Bitter-Suermann. "Anaphylatoxins." In Complement in Health and Disease, 299–324. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-2214-6_11.

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Müller, Thomas F., Christine M. Neumann, Christoph Greb, Michael Kraus, and Harald Lange. "The anaphylatoxin C5a, a new parameter in the diagnosis of renal allograft rejection." In Transplant International, 58–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-00818-8_16.

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Bosmann, Markus, and Peter A. Ward. "Role of C3, C5 and Anaphylatoxin Receptors in Acute Lung Injury and in Sepsis." In Advances in Experimental Medicine and Biology, 147–59. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0106-3_9.

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Vlattas, I., I. I. Sytwu, J. Dellurefïcio, J. Stanton, A. F. Braunwalder, N. Galakatos, R. Kramer, et al. "Identification of a receptor binding region in the core segment of the human anaphylatoxin C5a." In Peptides 1994, 105–6. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-1468-4_38.

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Moskopp, D., and L. Nocke-Finck. "Provisional Diagnostic Value of the Anaphylatoxin Radioimmunoassay (C3a-desArg-RIA) in the Neurosurgical Intensive Care Unit." In Advances in Neurosurgery, 328–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71108-4_54.

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Bischoff, S. C., Y. Kurimoto, and C. A. Dahinden. "Interleukin-3 and Granulocyte/Macrophage Colony-Stimulating Factor Change the Anaphylatoxin-Induced Basophil Mediator Release Pattern." In New Trends in Allergy III, 161–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-46717-2_23.

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Rohrer, Bärbel. "Anaphylatoxin Signaling in Retinal Pigment and Choroidal Endothelial Cells: Characteristics and Relevance to Age-Related Macular Degeneration." In Retinal Degenerative Diseases, 45–51. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75402-4_6.

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Conference papers on the topic "Anaphylatoxin"

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Rampart, M., H. Bult, A. G. Herman, P. J. Jose, and T. J. Williams. "PROSTACYCLIN (PGI2) FORMATION IN RELATION TO ANAPHYLATOXIN C5a GENERATION DURING RABBIT ENDOTOXIN SHOCK." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642837.

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Injection of endotoxin (LPS) in animals, a model for gram-negative septic shock, leads to intravascular activation of the complement system, and is one of the few conditions in which 6-oxo-PGF]CX and thromboxane (TX) B2 (non-enzymic metabolites of PGI2 and TXA2) can be detected in arterial blood. Previously we reported associations between complement activation, PGI2 biosynthesis and LPS-induced hypotension in rabbits. As C5a and C5adesArg trigger endothelial PGI2 formation in vitro, we have now measured the plasma levels of immunoreactive (ir) C5a in relation to generation of PGI2 and changes in arterial blood pressure in LPS shock. Pentobarbitone anaesthethized rabbits received LPS (E. coli 0111:B4, 0.5 mg/kg) or saline via the marginal ear vein. A catheter in the left carotid artery was used to collect blood and to monitor mean arterial blood pressure (MABP). Platelet and leukocyte numbers, haemolytic complement titre (CH50), and plasma ir6-oxo-PGFioc , irTXB2 and irC5a were measured 15 min before and at different times after saline or LPS injection. LPS caused a dose- and time-dependent formation of irC5a in rabbit serum in vitro, predominantly via the classical pathway. LPS also activated complement in vivo, as indicated by about 20 % reduction of CH50 titre (measured after 3h) and a marked increase of arterial irC5a (20-120 ng/ml) in the first 2 to 5 min. After 30 min, irC5a had returned to baseline levels (< 2-5 ng/ml) and remained so up to 3h after injection of LPS. This irC5a peak correlated with a shortlasting initiation of PGI2 release (from < 20 pg/ml up to 550 pg/ml) and a drop in MABP (from about 95 mmHg to 50 mmHg) 2-5 min after LPS. None of these changes occurred after saline injection.In conclusion, LPS activates complement in vivo with concomitant formation of C5a. This peptide may trigger -either directly or after phagocyte activation - endothelial PGI2 biosynthesis, leading to arterial hypotension. This is supported by the suppression of the initial rise of arterial ir6-oxo-PGF1α and hypotension in complement-depleted rabbits. Inhibition of C5a formation or activity may prove to be a meaningful approach to the treatment of septic circulatory shock.
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Mulligan, Jennifer, Sarah Casey, Ryan Mulligan, Tucker Williamson, Gary Gilkeson, Rodney Schlosser, and Carl Atkinson. "Inhibition Of The Complement Anaphylatoxin, C3a, Signaling Reduces Inflammation In A Murine Model Of Atopic Chronic Rhinosinusitis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4196.

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Tang, W., X. Li, L. Luo, X. Hu, S. Deng, B. Zhao, C. Hu, and J. Feng. "Anaphylatoxin C3a Enhances Recruitment of Monocytes Via Promoting the Production of Opsonins by Pleural Mesothelial Cells in Tuberculous Pleurisy." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6159.

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Casey, Sarah, Fei Qiao, Tucker Willamson, Gary Gilkeson, Stephen Tomlinson, and Carl Atkinson. "Complement Anaphylatoxins, C3a And C5a, Enhance Pro-Inflammatory Cytokine Production During Cigarette Smoke Induced Inflammation." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1296.

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Swaisgood, Carmen M., Lisa M. Ruple, and Daniel A. Culver. "Complement Anaphylatoxins C3a And C5a Increase In The BAL Of Mice At The Peak Of Lung Granuloma Formation Using The Mycobacterial Antigen SodA." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4520.

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