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Dissertationen zum Thema „Anaphylatoxin“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

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1

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 K_d 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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2

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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3

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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4

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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5

Püschel, Gerhard P., Ursula Hespeling, Martin Oppermann und 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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6

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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7

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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8

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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9

Püschel, Gerhard P., Martin Oppermann, Waldemar Muschol, Otto Götze und 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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10

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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11

Gervasoni, James Edmund Jr. „Degradation of Human Anaphylatoxin C3a by Rat Peritoneal Mast Cells: A Role for the Secretory Granule Enzyme Chymase and Heparin Proteoglycan“. VCU Scholars Compass, 1986. http://scholarscompass.vcu.edu/etd/4623.

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Purified human C3a was iodinated (125I-C3a) and used to study the interaction of labeled peptide with rat peritoneal mast cells (RMC). Cellular binding of 125I-C3a occurred within 30 sec, followed by a rapid dissociation from the cell. Both the binding of 125I-C3a and the rate of dissociation from the cell were temperature dependent. At 0°C, the binding of 125I-C3a was increased and the rate of dissociation reduced, as compared to 37°C. Once 125I-C3a was exposed to RMC, it lost the ability to rebind to a second batch of RMC. Analysis of the supernatants by trichloroacetic acid (TCA) precipitation and electrophoresis in sodium dodecyl sulfate polyacrylamide gels (SDS PAGE) revealed a decrease in the fraction of 125I precipitable by TCA and the appearance of 125I-C3a cleavage fragments. Pretreatment of RMC with enzyme inhibitors specific for chymotrypsin, but not trypsin, abrogated the degradation of 125I-C3a. Treatment of RMC bearing 125I-C3a with Bis (sulfosuccinimidyl) suberate (BS3) covalently crosslinked the 125I-C3a to chymase, the predominant enzyme found in the secretory granules. Antiserum directed against chymase precipitated 125I-C3a from extracts of RMC treated with BS3. Indirect immunofluorescence of RMC using the 1gG fraction of goat anti-rat chymase showed that chymase is present on the surface of unstimulated cells. Neither purified chymase nor heparin proteoglycan alone had any appreciable effect on 125I-C3a, but together they resulted in prompt degradation of the 125I-C3a. Immunoabsorption of RMC sonicates with specific antibody for chymase completely abrogated the ability of these sonicates to degrade 125I-C3a. Intact RMC were pretreated with serine esterase inhibitors prior to 125I-C3a and BS3 exposure. The cells to which 125I-C3a had been crosslinked to were solublized and analyzed by SDS PAGE and autoradiography. There were three bands visualized, a 35,000 dalton band which was defined as chymase, and two undefined 45,000 and 55,000 dalton bands. The results indicate that 125I-C3a binds to RMC and is promptly degraded by chymase in the presence of heparin proteoglycan. In addition, this proteolysis of 125I-C3a by chymase must be blocked in order to detect plasma membrane C3a binding components on RMC.

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12

Kusakabe, Jiro. „Complement 5 inhibition ameliorates hepatic ischemia/reperfusion injury in mice, dominantly via the C5a-mediated cascade“. Kyoto University, 2020. http://hdl.handle.net/2433/254516.

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13

Püschel, Gerhard P., Martin Oppermann, Frank Neuschäfer-Rube, Otto Götze und Kurt Jungermann. „Differential effects of human anaphylatoxin C3a on glucose output and flow in rat liver during orthograde and retrograde perfusion : the periportal scavenger cell hypothesis“. Universität Potsdam, 1991. http://opus.kobv.de/ubp/volltexte/2008/1674/.

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1) During orthograde perfusion of rat liver human anaphylatoxin C3a caused an increase in glucose and lactate output and reduction of flow. These effects could be enhanced nearly twofold by co-infusion of the carboxypeptidase inhibitor MERGETPA, which reduced inactivation of C3a to C3adesArg. 2) During retrograde perfusion C3a caused a two- to threefold larger increase in glucose and lactate output and reduction of flow than in orthograde perfusions. These actions tended to be slightly enhanced by MERGETPA. 3) The elimination of C3a plus C3adesArg immunoreactivity during a single liver passage was around 67%, irrespective of the perfusion direction and the presence of the carboxypeptidase inhibitor MERGETPA; however, less C3adesArg and more intact C3a appeared in the perfusate in the presence of MERGETPA in orthograde and retrogade perfusions It is concluded that rat liver inactivated human anaphylatoxin C3a by conversion to C3adesArg and moreover eliminated it by an additional process. The inactivation to C3adesArg seemed to be located predominantly in the proximal periportal region of the liver sinusoid, since C3a was less effective in orthograde perfusions, when C3a first passed the proximal periportal region before reaching the predominant mass of parenchyma as its site of action, than in retrograde perfusions, when it first passed the perivenous area. These data may be evidence for a periportal scavenger mechanism, by which the liver protects itself from systemically released mediators of inflammation that interfere with the local regulation of liver metabolism and hemodynamics.

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14

Koleva, Milena. „De-novo-Induktion von Anaphylatoxin-C5a-Rezeptoren in Hepatocyten der Ratte durch den Entzündungsauslöser Lipopolysaccharid in vivo Vermittlung durch die Entzündungsmediatoren Interleukin-6 und -1[beta] /“. [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=965256928.

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15

Quell, Katharina Maria [Verfasser], Yves [Akademischer Betreuer] Laumonnier und Hauke [Akademischer Betreuer] Busch. „The role of the anaphylatoxin receptors C3aR, C5aR1 and C5aR2 on alveolar macrophages in experimental allergic asthma / Katharina Maria Quell ; Akademische Betreuer: Yves Laumonnier, Hauke Busch“. Lübeck : Zentrale Hochschulbibliothek Lübeck, 2020. http://d-nb.info/121491439X/34.

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16

Giannini, Eric. „Étude de la désensibilisation du récepteur de la fraction C5a dans les polynucléaires neutrophiles“. Grenoble 1, 1995. http://www.theses.fr/1995GRE10142.

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La fixation de l'anaphylatoxine c5a sur son recepteur conduit a la fois a la stimulation des reponses cellulaires (production de superoxyde, degranulation) et a la desensibilisation du recepteur dans les cellules myeloides. La phosphorylation du recepteur apparait etre une etape cle dans la regulation de la transduction du signal a partir de ces recepteurs. Alors que la transmission du signal via des proteines g sensibles a la toxine de bordetella pertussis est necessaire a l'activation du neutrophile, la phosphorylation du recepteur, est quant a elle independante de cette voie. Cette phosphorylation est un processus transitoire indiquant une etape de dephosphorylation. De plus quelques minutes apres la phosphorylation, rc5a est internalise. Cette internalisation est suivie d'un recyclage du recepteur a la membrane avec une cinetique comparable a celle de la dephosphorylation, cette derniere pouvant etre cruciale pour le recyclage et la resensibilisation. La mutagenese de recepteur au niveau des sites de phosphorylation conduit a des recepteurs dont le niveau de phosphorylation est fortement diminue, et incapables de se desensibiliser

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17

Hespeling, Ursula, Gerhard Püschel, Kurt Jungermann, Otto Götze und Jörg Zwirner. „Stimulation of glycogen phosphorylase in rat hepatocytes via prostanoid release from Kupffer cells by recombinant rat anaphylatoxin C5a but not by native human C5a in hepatocyte/Kupffer cell co-cultures“. Universität Potsdam, 1995. http://opus.kobv.de/ubp/volltexte/2010/4590/.

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Human anaphylatoxin C3a had previously been shown to increase glycogenolysis in perfused rat liver and prostanoid formation in rat liver macrophages. Surprisingly, human C5a, which in other systems elicited stronger responses than C3a, did not increase glycogenolysis in perfused rat liver. Species incompatibilities within the experimental system had been supposed to be the reason. The current study supports this hypothesis: (1) In rat liver macrophages that had been maintained in primary culture for 72 h recombinant rat anaphylatoxin C5a in concentrations between 0.1 and 10 pg/ml increased the formation of thromboxane A₂, prostaglandin D₂, E₂ and F₂α6- to 12-fold over basal within 10 min. In contrast, human anaphylatoxin C5a did not increase prostanoid formation in rat Kupffer cells. (2) The increase in prostanoid formation by recombinant rat C5a was specific. It was inhibited by a neutralizing monoclonal antibody. (3) In co-cultures of rat hepatocytes and rat Kupffer cells but not in hepatocyte mono-cultures recombinant rat C5a increased glycogen phosphorylase activity 3-fold over basal. This effect was inhibited by incubation of the co-cultures with 500 μM acetylsalicyclic acid. Thus, C5a generated either locally in the liver or systemically e.g. in the course of sepsis, may increase hepatic glycogenolysis by a prostanoid-mediated intercellular communication between Kupffer cells and hepatocytes.

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18

Crass, Torsten. „Die Anaphylatoxine C3a und C5a und ihre zellulären Rezeptoren molekulare Untersuchungen zur Ligand-Rezeptor-Interaktion ; 1. Molekulare Klonierung und Charakterisierung des humanen C3a-Rezeptors, 2. Generierung und Charakterisierung von C3a-Rezeptor-/C5a-Rezeptor-Chimären, 3. Charakterisierung von C-terminalen C5a-Mutanten /“. [S.l. : s.n.], 1999. http://deposit.ddb.de/cgi-bin/dokserv?idn=957116462.

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19

Westwood, J. P. „The role of complement anaphylatoxins in systemic disease“. Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1470035/.

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The complement system has a vital role both in innate and adaptive immunity. Study of diseases associated with defective complement regulation has shown the harmful effects of inappropriate and/or excessive complement activation to the host organism. The hypothesis for this thesis is that complement activation is a feature of the acute phase of several disorders, and that complement overactivation - characterized by high levels of the anaphylatoxins C3a and C5a - has a pathological role, with high levels being associated with a worse prognosis. Complement anaphylatoxins were measured in patients hospitalized with community acquired pneumonia, and patients with exacerbations of chronic obstructive pulmonary disease (COPD). Patients with thrombotic thrombocytopenic purpura (TTP) were also studied in detail: following a retrospective review of the role of immunosuppression with rituximab in these patients, a prospective study was performed to compare complement levels in acute disease with remission cases. Complement activation was present in the acute phase of all diseases studied, but there was a considerable variation in levels between cases. High systemic levels of complement anaphylatoxins were seen in several patients, but there was no clear association with prognosis; however in patients with COPD changes in sputum complement levels were associated with a longer time to clinical recovery. Patients with TTP generally had higher levels during the acute phase of the disease, and a positive correlation was found between complement activation and the level of antibody mediating the disease.

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20

Khan, Nazmin. „The role of anaphylatoxins in asthma and airway remodelling“. Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-anaphylatoxins-in-asthma-and-airway-remodelling(ee2de1d0-eb02-4b19-b546-2d4c26d4bbef).html.

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C3a and C5a anaphylatoxins are proinflammatory polypeptides released during complement activation. They exert their biological functions by interacting with the G protein-coupled receptors, C3aR and C5aR respectively. Activation of the complement system has been implicated in the pathogenesis of many inflammatory diseases including asthma. Little is known, however, about the expression and location of complement components in asthmatic airways. -- Experiments described in this thesis demonstrate the expression and localisation of certain complement components and their two receptors in the bronchial mucosa. C3a and C5a-stimulated production of remodelling mediators and the biological function of the anaphylatoxins on the structural cells was also assessed. -- Immunohistochemical analysis revealed elevated expression/deposition of C3 and C5 components in the epithelium, airway smooth muscle and submucosa of asthmatics compared with controls, and also demonstrated expression of the two complement receptors on airways structural cells, including airway epithelial cells, endothelial cells, fibroblasts and smooth muscle cells (SMC). -- In general C3a was the more effective of the two anaphylatoxins in inducing structural cellular proliferation: C3a increased fibroblast and endothelial cell proliferation at a range of concentrations embracing the physiological, although it increased SMC proliferation only at the highest concentration (10~7 M) employed, and epithelial cell proliferation only at the lowest concentration (10~9 M) employed. C5a induced fibroblast proliferation but had no effect in this regard on the other structural cells.

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21

Bälder, Ralf. „Die Bedeutung der Anaphylatoxine C3a und C5a im Mausmodell der allergischen Atemwegsentzündung“. [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=973165596.

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22

Ingersoll, Sarah. „The role of complement anaphylatoxins in CNS pathology and glial cell function“. Diss., University of Iowa, 2010. https://ir.uiowa.edu/etd/823.

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Demyelination in the CNS is known to involve several immune effector mechanisms, including complement proteins. For this dissertation project the central hypothesis that C3 and downstream effector complement proteins exacerbate demyelination through activation of glial cells was tested. To investigate the role of C3 and downstream complement proteins in demyelination and remyelination pathology in vivo we utilized the cuprizone model. We used C3 knockout mice (C3-/-), which are lacking the central C3 protein and subsequently all downstream complement effector proteins, and transgenic mice expressing C3a or C5a under the control of the glial GFAP promoter. Interestingly, we found no changes in demyelination or remyelination pathology between C3-/- and control mice. However, C3a and C5a transgenic mice had exacerbated demyelination and slightly delayed remyelination in the corpus callosum compared to WT mice. Transgenic mice had increased cellularity in the corpus callosum due to increased activation and/or migration of microglia. There was also evidence of T cells in the corpus callosum during demyelination in C5a transgenic mice, suggesting C5a may modulate BBB permeability. During early remyelination oligodendrocytes migrated to the corpus callosum in higher numbers in C3a and C5a transgenic mice, thus enabling these mice to remyelinate as effectively as WT mice by the end of the ten week study. To determine the effects of anaphylatoxins on individual glial subsets, we created murine recombinant C3a and C5a proteins. We found that the MAPK pathway proteins JNK1 and ERK1/2 were activated in glia upon stimulation with recombinant anaphylatoxin proteins. When microglia and mixed glial cultures were stimulated with C3a and/or C5a, we observed an increase in the production of proinflammatory cytokines and chemokines. In contrast, anaphylatoxin-treated primary astrocytes had suppressed cytokine and chemokine production compared to untreated astrocytes. In vitro, primary microglia and astrocytes did not significantly migrate in response to stimulation with C3a or C5a proteins, suggesting migration may not be a primary anaphylatoxin-mediated function in the CNS. Overall, our findings show that anaphylatoxin production in the brain plays a negative proinflammatory role during demyelination and that anaphylatoxin proteins can activate individual subsets of glia, initiating the production of inflammatory mediators.

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23

Figge, Julia [Verfasser]. „Die Bedeutung des Anaphylatoxins C5a für die Funktion von B-Lymphozyten / Julia Figge“. Lübeck : Zentrale Hochschulbibliothek Lübeck, 2013. http://d-nb.info/1043583203/34.

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24

Chatagner, Alexandra. „Complément et neuroprotection“. Rouen, 2005. http://www.theses.fr/2005ROUES037.

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Pendant longtemps, l'activation du complément exprimé dans le système nerveux central a été considérée comme délétère pour les cellules environnantes puisque permettant une amplification de l'inflammation et surtout la lyse cellulaire par le complexe d'attaque membranaire. Mais le concept d'un rôle du complément dans la neuroprotection a émergé suite à des données plus récentes. Le travail de cette thèse a consisté à explorer les mécanismes que le complément met en place également par son activation pour protéger les cellules avoisinantes, les neurones essentiellement. Cela peut passer par une augmentation d'expression de CD55 au niveau neuronal ou par la libération de NGF par les astrocytes grâce à un effet synergique des anaphylatoxines et IL-1b. En revanche, la phagocytose des cellules en apoptose, processus important pour éviter le déclenchement d'un réaction inflammatoire n'est pas régulée par le C3a
For a long time, the classical dogma has considered complement activation in brain pathology deleterious for surrounding cells since it promotes inflammation processes and triggers membran attack complexe formation resulting in cell lysis. A growing body of evidence implicates complement in neuoroprotection processes. My PhD work consisted in exploring the different mecanisms set up by complement activation to protect cells, neurons essentially. The up-regulation of neuronal CD55 or NGF secretion by astrocytes following a simultaneous anaphylatoxins and IL-1b stimulation may contibute to neuronal protection. On the other hand, phagocytosis of apoptotic cells, which is an important process to prevent inflammatory reaction is not regulated by C3a

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Karbach, Michael [Verfasser]. „Die Rolle des Anaphylatoxins C5 in der Pathogenese des Trauma-induzierten septischen akuten Lungenschadens / Michael Karbach“. Ulm : Universität Ulm, 2020. http://d-nb.info/1221671162/34.

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Stott, Matthew. „Activation and inactivation of the complement anaphylatoxins during chronic neutrophilic inflammation of the cystic fibrosis airway“. Thesis, Cardiff University, 2018. http://orca.cf.ac.uk/118523/.

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Cystic fibrosis (CF) is a fatal genetic disease that affects 1/2500 people in the UK. Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) cause dehydration of mucosal membranes, leading to mucus obstruction of the small airways. The CF lungs are susceptible to recurrent infection promoting chronic neutrophilic inflammation. Neutrophils recruited to the CF lungs become dysfunctional and are ineffective at clearing pathogens, perpetuating inflammation. Neutrophil serine proteases (NSPs) released by neutrophils collaterally remodel the airway, reducing lung function and causing mortality. The complement anaphylatoxins (C5a and C3a) are important mediators of inflammation. C5a and C3a are chemotactic for monocytes and granulocytes, they also stimulate degranulation and the generation of reactive oxygen species (ROS). C5a is particularly potent towards neutrophils and is critical for orchestrating their response towards pathogens. C5a and C3a are elevated in the CF airway. Furthermore, in addition to complement activation these anaphylatoxins can be generated by non-complement proteases including NSPs. The mechanisms by which C5a and C3a promote chronic neutrophilic inflammation in the CF airways are not fully understood. In my study I show that C5a and C3a correlate with markers of neutrophilic inflammation (neutrophil count and CXCL8) in bronchoalveolar lavage (BAL) fluid from paediatric CF patients. I further characterise the generation of functionally active C5a-like and C3a-like forms by NSPs. Moreover, I demonstrate that atypical C5a production by NSPs cannot be prevented by therapeutic complement inhibitors. I show for the first time that NSP-generated C5a-like fragments are resistant to inactivation by carboxypeptidase B, an important regulator of C5a activity. I also further characterise the interaction between C5a and soluble glycosaminoglycans (GAGs), these are abundant during chronic neutrophilic inflammation of the CF airway. Additionally, I show that GAG interaction influences C5a activity. In conclusion, the CF airway environment modifies C5a function; these mechanisms could promote chronic neutrophilic inflammation.

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Jauneau, Anne-Christine. „Complément et système nerveux central, rôles des anaphylatoxines C3a et C5a au niveau de l'astrocyte“. Rouen, 2002. http://www.theses.fr/2002ROUES063.

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Le cerveau peut être le siège d'une réaction inflammatoire au cours de nombreuses pathologies durant lesquelles une augmentation de la synthèse du complément, acteur majeur de l'immunité naturelle, a pu être observée. En l'absence de tout infiltrat cellulaire, une réaction inflammatoire intrinsèque peut être réalisée par les cellules gliales. L'activation de ces cellules, qui synthétisent la totalité des composants de la cascade du complément aboutit, notamment, à la libération des anaphylotoxines C3a et C5a, deux puissants médiateurs inflammatoires, ainsi qu'à la formation du complexe d'attaque membranaire. La mise en évidence des récepteurs des anaphylatoxines à la surface des cellules du cerveau et l'observation d'une augmentation de leur expression au cours de certaines pathologies nous a mené à examiner leurs rôles au sein du cerveau, et en particulier au niveau des astrocytes, cellules gliales aux propriétés immunocompétentes. Au cours de ces travaux, nous montrons que le C3a et le C5a entraînent l'activation de plusieurs voies de transduction aboutissant à une augmentation de l'expression des ARNm de chimiokines parmi lesquelles l'IL-8. En revanche, une augmentation de la sécrétion d'IL-8 par les anaphylotoxines n'a pu être observée qu'en présence d'IL-1ß. Ainsi, les anaphylotoxines participeraient, au moins partiellement, au recrutement des leucocytes au sein du cerveau. Le C3a et le C5a augmentent également l'expression des ARNm de certaines neurotrophines ainsi qu'une sécrétion modeste du NGF, participant ainsi aux phénomènes de neuroprotection et de réparation post-lésionnelle. Enfin, nous montrons un rôle tout à fait inattendu du C3a dans l'élimination des cellules apoptotiques via l'augmentation de l'expression du récepteur à la phosphatidylsérine au niveau des astrocytes. L'ensemble de ces travaux, effectués au niveau de l'astrocyte, attribue de nouveaux rôles aux anaphylatoxines et suggère qu'au niveau du cerveau elles exerceraient un effet dualiste
Inflammatory reactions could occur in the brain during numerous pathological disorders when an increase of complement synthesis, actor of natural immunity, has been observed. In the absence of cellular infiltration, an intrathecal inflammatory reaction could be realized by glial cells. The activation of these cells, which synthesize the totality of the complement cascade components, leads to the release of C3a and C5a anaphylatoxins, two potent inflammatory mediators, and to the formation of the membrane attack complex. The presence of anaphylatoxin receptors on brain cells and the increase of their expression during some pathologies led us to determine their roles in the brain, in particular on astrocytes, immunocompetent glial cells. Our studies show that C3a and C5a activate several transduction pathways leading to an increase of chemokine mRNA expression, including IL-8. However an increase of IL-8 secretion could be detected only in the presence of IL-1ß. Thus, at least in part, anaphylatoxins may participate to leukocyte recruitment into the brain. C3a and C5a also increase neurotrophin mRNA expression and lead to a weak secretion of NGF, and so, participate to neuroprotection and post-lesioned repairing. Finally, we show an unexpected role for C3a in the clearance of apoptotic cells via the increase of phosphatidylserine receptor expression by astrocytes. Our data allocate new roles to anaphylatoxins on astrocytes and suggest that they could have a dual effect in the brain

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Bröker, Katharina [Verfasser]. „Die Rolle des Anaphylatoxins C5a und seiner Rezeptoren in der Biologie der B-1-Lymphozyten / Katharina Bröker“. Lübeck : Zentrale Hochschulbibliothek Lübeck, 2017. http://d-nb.info/1129726371/34.

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Poursharifi, Pegah. „Immunometabolic aspect of C5L2 and C5aR in adiposity : physical, functional and physiological interactions“. Doctoral thesis, Université Laval, 2014. http://hdl.handle.net/20.500.11794/25593.

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L’obésité est maintenant reconnue comme présentant une inflammation chronique et est caractérisée par une augmentation de l’infiltration de macrophages dans le tissu adipeux. Cette infiltration est réflètée par l’activation du système du complément qui agit comme élément déclencheur et précurseur aux autres fonctions immunitaires. Le C5L2 (C5aR-like receptor 2) a récemment été identifié comme récepteur pour la protéine stimulant l’acylation (ASP) ainsi que pour le facteur inflammatoire C5a (capable quant à lui d’aussi se lier au C5aR). Cette thèse porte sur: (i) l’interaction entre C5L2 et C5aR suite à l’activation de ceux-ci par leurs ligands respectifs dans des lignées cellulaires adipocytaires (3T3-L1) et de macrophages (J774), (ii) la contribution du C5aR au métabolisme et à la réponse immunitaire d’adipocytes provenant de modèles murins et (iii) l’association entre C5L2 et C5aR avec des facteurs reliés à l’obésité chez l’humain. Les récepteurs C5L2 et C5aR s’associent entre-eux de façon constitutive en homo- et hétérodimères et l’ajout de ligand à des cultures d’adipocytes 3T3-L1 ou de macrophages J774 augmente cette colocalisation. Autant l’ASP que le C5a ont réussi à induire une réponse fonctionnelle chez des adipocytes primaires. Lorsque des adipocytes primaires provenaient de souris invalidées pour le C5aR, les effets d’un traitement avec C5a étaient perturbés tandis que les effets médiés par un traitement à l’ASP étaient maintenus. De plus, l’addition de C5a bloquait la signalisation et la réponse fonctionnelle causées par un traitement à l’ASP chez les adipocytes primaires provenant de souris C5aRKO et de type sauvage. Finalement, l’expression des gènes C5L2 et C5aR dans le tissu adipeux de femmes obèses morbides était associée avec une adiposité croissante. De façon interessante, les ratios ASP/C5L2 et C5L2/C5aR augmentaient de façon significative avec l’obésité abdominale. Lorsque pris ensemble, l’interaction fonctionelle, physiologique et la proximité physique des récepteurs C5L2 et C5aR chez les adipocytes suggèrent un rôle potentiel de ceux-ci sur l’immunométabolisme du tissu adipeux. De surcroit, cette interaction met en valeur les liens qui existent entre le tissu adipeux et les protéines et récepteurs du complément tout en démontrant comment une réponse excessive au niveau immuno-métabolique pourrait exacerber le développement du niveau d’adiposité chez l’individu.
From the convergence of metabolism and immune research has emerged a new research field, termed “Immunometabolism”. Obesity, an immunometabolic disease, is associated with a state of low-grade inflammation and is characterized by increased infiltration of macrophages into adipose tissue. Complement activation can act as an early trigger and precursor of other immune functions. C5aR-like receptor 2 (C5L2) has been identified as a receptor for Acylation Stimulating Protein (ASP) and the inflammatory factor C5a (which can also bind C5aR). This thesis sequentially evaluates (i) ligand-induced C5L2 and C5aR interaction in cultured 3T3-L1 adipocytes and J774 macrophages, (ii) the C5aR contribution in adipocyte metabolic and immune responses in mouse models, (iii) as well as C5L2 and C5aR association with obesity-related factors in humans. The immunometabolic receptors, C5L2 and C5aR, constitutively self-associate into homo-/heterodimers and ligand treatment of 3T3-L1 adipocytes and J774 macrophages increased their colocalization. Both C5a and ASP directly induced primary adipocyte signaling and function. However, in C5aRKO primary adipocytes, C5a effects were disrupted, while stimulatory effects of ASP were mostly maintained. Moreover, addition of C5a completely blocked ASP signaling and activity in both C5aRKO and WT primary adipocytes. Finally, C5L2 and C5aR expression in adipose tissue from morbidly obese women was associated with increased adiposity. Interestingly, ASP/C5L2 and C5L2/C5aR ratio markedly increased with abdominal obesity. Taken together, the closely linked physical, functional and physiological interaction between C5L2 and C5aR in adipocytes suggests a potential role in adipose tissue immunometabolism. This further highlights the important new links between adipose tissue and complement proteins/receptors and demonstrates how excessive immunometabolic responses may exacerbate adiposity.

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Bénard, Magalie. „Étude du rôle des récepteurs des anaphylatoxines C3a et C5a dans le remodelage et le développement tissulaires“. Rouen, 2007. http://www.theses.fr/2007ROUES013.

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Les anaphylatoxines du complément et leurs récepteurs, RC3a et RC5a, jouent un rôle lors de la régénération et l’ontogénèse tissulaires. Les hépatocytes n’expriment le RC5a qu’après un stress inflammatoire ; l’administration de C5a augmente la prolifération hépatocytaire in vitro et in vivo, au cours de la régénération hépatique. Les RC3a et RC5a sont exprimés dans les neurones en grain du cervelet de rat en cours de développement. In vitro, le RC5a protège les neurones en grain de l’apoptose induite par appauvrissement du milieu ; in vivo, l’injection sous durale de C5a induit une prolifération accrue des neuroblastes par une action directe sur le RC5a neuronal. L’injection de C3a provoque une diminution de la couche externe du cervelet et une augmentation concomitante de celle de la couche interne pouvant s’expliquer par une accélération de la migration des neurones en grain comme mesurée in vitro par une augmentation de la motilité des neuroblastes
Complement anaphylatoxines and their receptors, C3Ar and C5aR, play a role in regeneration and ontogenesis. Hepatocytes express C5aR only after inflammatory stress. C5a administration increase the hepatocyte proliferation in vitro and in vivo, during liver generation. C3aR and C5aR are expressed in granular neurons of rat cerebellum during development. In vitro, C5aR protects granular neurons against apoptosis induced by lack of substract in medium ; in vivo, sub-dural injection of C5a induces an increase of neuroblast proliferation by a direct action of this peptide on C5aR. C3a injection provokes a decrease of cerebellar external layer and a concomitant increase of internal layer that could be explained by an acceleration of granular neuron migration as measured in vitro by an increase of neuroblast motility

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Girke, Georg [Verfasser]. „Komplementaktivierung in der Sehne : Wirkung des Anaphylatoxins C3a und des in-vitro Sehnenverletzungsmodells auf Tendozyten vor dem Hintergrund der Sehnenheilung / Georg Girke“. Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2014. http://d-nb.info/1051812216/34.

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Thorel, Nathalie. „Rôle du complément dans la réaction inflammatoire gliale : contribution à l'étude du CR2/CD21 et du GPR176“. Rouen, 2009. http://www.theses.fr/2009ROUES041.

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Dans le but d'approfondir le rôle des anaphylatoxines dans le système nerveux central, nous avons stimulé des cellules T98G par le C3a ce qui a conduit à la découverte de deux molécules. Le CR2 est présent sur les astrocytes mais sa fonction est inconnue. Nous avons produit un anticorps monoclonal capable d'activer le CR2 astrocytaire qui s'associe à TAPA-1 et à la caldesmone qui sont connus pour arrêter la prolifération cellulaire. Ensuite, nous avons étudié le GPR176 dont le ligand est inconnu. Des animaux ont été immunisés selon quatre protocoles mais nous n'avons pas pu obtenir d'anticorps. Le GPR176 est principalement exprimé au niveau du système nerveux. Nous avons produit une lignée stable qui permettra de découvrir son ligand. L'ensemble de ces résultats ne nous a pas permis de corréler le complexe CR2/TAPA-1 et le GPR176 avec la réaction inflammatoire gliale mais les résultats obtenus sur le CR2 supposent une action de ce récepteur dans la formation de la cicatrice gliale
In order to decipher the function of anaphylatoxins in the central nervous system, we stimulated glioblastomas cells with C3a which leads us to the discovery of two molecules induced by C3a. CR2 is expressed on astrocytes but its function is unknown. We produced a monoclonal antibody which can activate astrocytic CR2 which translocates with TAPA-1 and with the non-muscle caldesmon. These proteins are known to arrest cell migration. In a second part, we study the GPR176 whose ligand is unknown. We immunized rabbits and mice with four protocols but we failed to obtain an antibody. We localized GPR176 in the central nervous system and particularly in the lombar spinal cord and in locus coeruleus. We produced a stable cell line which will be used in ligand finding. These results don't show an interaction between the complex TAPA-1/CR2 and GPR176 with glial inflammation but findings obtained with CR2 suppose a role of this receptor in promoting glial scar formation

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Tom, Fun-Qun. „Effets de la protéine stimulant l'acylation dans l'interaction des adipocytes et des macrophages“. Thesis, Université Laval, 2011. http://www.theses.ulaval.ca/2011/28657/28657.pdf.

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Sayah, Sakina. „Implication du complément dans les mécanismes inflammatoires du système nerveux central : expression des récepteurs des anaphylatoxines C3a (C3aR) et C5a (C5aR) par les astrocytes“. Rouen, 1998. http://www.theses.fr/1998ROUES081.

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Le système nerveux central (SNC) peut être le siège de réactions inflammatoires au cours de diverses pathologies. De nombreux acteurs cellulaires et moléculaires participent à l'initiation et à l'amplification de l'inflammation cérébrale. Ainsi, les cellules gliales du SNC et les cellules immunes infiltrantes sont responsables de la production de cytokines et de protéines du complément (C) observée dans le cerveau pathologique. Plusieurs études ont montré l'implication du C dans les pathologies du SNC. Les anaphylatoxines C3a et C5a sont deux peptides pro-inflammatoires libérés lors de l'activation du C. Elles agissent par l'intermédiaire de récepteurs spécifiques respectivement nommes C3aR et C5aR. Nous avons émis l'hypothèse que C3a et C5a libérées dans le cerveau pourraient exercer leurs effets inflammatoires via leur liaison au C3aR et au C5aR sur les cellules nerveuses. L'astrocyte, cellule gliale du SNC, a constitué notre modèle d'étude car cette cellule possède un étonnant potentiel immunologique et est fortement impliquée dans l'inflammation cérébrale. Notre étude a été menée en parallèle sur des lignées astrocytaires humaines et sur des astrocytes de rat en culture primaire. Nous avons montré l'expression constitutive des récepteurs C3aR et C5aR à la surface des astrocytes. Les deux récepteurs sont fonctionnels puisque leur stimulation par C3a et C5a induit d'une part l'activation de voies de transduction et, d'autre part, une augmentation de l'expression des ARNm des cytokines IL-6 et IL-8, et une sécrétion d'IL-8 par les astrocytes. L'ensemble de ces données nous permet d'attribuer de nouveaux rôles à C3a et C5a au sein du cerveau et renforce l'implication des anaphylatoxines dans les processus inflammatoires cérébraux et la pathogénèse du SNC.

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Delafontaine, Marie Paule Jacqueline. „Veneno da serpente Bothrops lanceolatus: caracterização, ativação do sistema complemento e mecanismos potenciais envolvidos no envenenamento“. Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-12092016-113750/.

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Na Martinica, os envenenamentos por Bothrops lanceolatus apresentam um quadro clínico trombótico, acompanhado de inflamação local extensa, envolvendo edema, dor e hemorragia limitada. Neste estudo foi mostrado que vários componentes do veneno compartilham similaridades antigênicas com venenos de espécies da América do Sul. O veneno de B. lanceolatus é citotóxico para queratinócitos e células endoteliais, induzindo a produção de citocinas e quimiocinas pro-inflamatórias pelas células. O veneno de B. lanceolatus ativa a cascata do complemento, liberando anafilatoxinas, assim como o complexo terminal do complemento. Ele apresenta uma ação proteolítica sobre os componentes purificados C3, C4, C5, e o inibidor de C1, C1-INH. O veneno também desequilibra o balanço de expressão dos reguladores do complemento na membrana das células endoteliais. Estes dados demonstram que o veneno de B. lanceolatus exibe uma potente ação proinflamatória, pela ativação do sistema complemento e pela sua toxicidade em células endoteliais.
In Martinique envenomations by Bothrops lanceolatus are characterized by a systemic thrombotic syndrome and important local inflammation, involving oedema and pain, but limited haemorrhage. In this study, we show that several components of B. lanceolatus venom share antigenic similarities with South American Bothrops species. Still, B. lanceolatus venom proteases present substrate specificity. The venom is cytotoxic for keratinocytes and endothelial vascular cells, inducing the production of pro-inflammatory cytokines and chemokines. B. lanceolatus venom activates the complement cascade, releasing anaphylatoxins and the terminal complement complex. It also shows a direct proteolytic activity upon the purified complement proteins C3, C4, C5, and the inhibitor of C1, C1-INH. B. lanceolatus venom modified the balance of complement regulators on endothelial cells membrane. In conclusion, B. lanceolatus venom displays important pro-inflammatory properties, as it activates the complement cascade and impacts endothelial cells.

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Christophe, Thierry. „Etude de la régulation du récepteur de l'anaphylatoxine C5a : identification de ligands des récepteurs de la famille FPR“. Université Joseph Fourier (Grenoble), 2000. http://www.theses.fr/2000GRE10229.

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Les leucocytes peuvent etre actives par des agents chimioattractants tels que des peptides bacteriens (fmlp) ou la fraction c5a du complement. Ces agents chimioattractants induisent la migration des leucocytes, leur degranulation et l'activation du complexe nadph oxydase qui produit les ions superoxyde impliques dans la destruction des pathogenes. Ces reponses cellulaires sont declenchees par la fixation de ces agents sur des recepteurs specifiques qui appartiennent a la superfamille des recepteurs couples aux proteines g heterotrimeriques. Malgre la presence continue d'agonistes, les reponses cellulaires sont transitoires et les cellules deviennent refractaires a une autre stimulation (desensibilisation homologue). Selon le concept actuel, le recepteur est phosphoryle, ce qui permet son interaction avec la proteine adaptatrice -arrestine. Cette interaction inhibe le couplage recepteur/proteine g et induit l'internalisation du recepteur par les puits recouverts de clathrine. Apres addition de c5a, le recepteur du c5a (rc5a) est phosphoryle sur six serines de la queue c-terminale intracellulaire. En utilisant des recepteurs dont certaines serines ont ete mutees, nous avons montre que : (1) cette phosphorylation suit un processus hierarchique, debutant par la phosphorylation des serines s334 et s332. (2) la phosphorylation de la serine s338 est necessaire au decouplage recepteur/proteine g. (3) le decouplage et l'internalisation de rc5a sont deux processus independants. (4) dans les cellules promyelocytaires hl-60, rc5a peut etre internalise par un mecanisme independant de la phosphorylation. Rc5a peut egalement etre internalise par la voie classique dependante de la phosphorylation. Ces deux mecanismes sont sensibles au dominant negatif de la dynamine, une gtpase qui intervient au niveau de la membrane dans la fermeture des vesicules d'endocytose, suggerant l'implication des puits recouverts de clathrine. D'autre part, nous avons identifie le peptide synthetique wkymvm comme un agoniste des recepteurs fpr, fprl1 et fprl2 ; wkymvm est specifique de fprl1 et fprl2. Un peptide antibacterien produit par helicobacter pylori (hp(2-20)) est egalement un agoniste de fprl1 et fprl2.

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Cao, Qi. „Expression and Role of Anaphylatoxin Receptors on Human Colonic Epithelial Cells“. 2012. http://hdl.handle.net/10222/21905.

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Human colonic epithelial cell lines (T84, Caco2 and HT-29) were used to address the question of whether intestinal epithelial cells can detect and respond to activated complement via the anaphylatoxin receptors, considering the gut is host to large numbers of bacteria. All cell lines possess C3aR, C5aR and C5L2. Confocal microscopy confirmed that cells express apical C5aR and C5L2. C3a and C5a up-regulated CXCL8 and CXCL10 mRNA but not secreted protein levels within 48 hours. Protein levels were not increased using simultaneous treatment with subthreshold concentrations of LPS or TNF plus anaphylatoxin. C3a and C5a also increased the permeability of polarized monolayers. Anaphylatoxins also promoted the proliferation of T84 and HT-29. Inhibition of ERK signaling abolished these effects of anaphylatoxins. Our findings that multiple human cell lines possess functional anaphylatoxin receptors indicates that the colonic epithelium likely responds to the activation of complement in the lumen with an inflammatory outcome.

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Kiafard, Ziba. „Herstellung und Charakterisierung monoklonaler Antikörper gegen die Anaphylatoxin-Rezeptoren“. Doctoral thesis, 2007. http://hdl.handle.net/11858/00-1735-0000-0006-ACEF-D.

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Weyergraf, Ansgar Johannes Elsner Jörn. „Expression und Regulation des Anaphylatoxin-C3a-Rezeptors auf humanen eosinophilen Granulozyten /“. 2005. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=014984241&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Kiafard, Ziba [Verfasser]. „Herstellung und Charakterisierung monoklonaler Antikörper gegen die Anaphylatoxin-Rezeptoren / vorgelegt von Ziba Kiafard“. 2008. http://d-nb.info/990160440/34.

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Koleva, Milena. „De novo Induktion von Anaphylatoxin C5a-Rezeptoren in Hepatocyten der Ratte durch den Entzündungsauslöser Lipopolysaccharid in vivo“. Doctoral thesis, 2001. http://hdl.handle.net/11858/00-1735-0000-0006-B604-A.

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Schaefer, Myriam [Verfasser]. „Analyse der transkriptionellen Regulation des C3a-Rezeptors & der Genexpression monozytärer Zellen nach Anaphylatoxin-Stimulation / von Myriam Schaefer“. 2004. http://d-nb.info/974105155/34.

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Klein, Lorenzo Wolfgang Klos Andreas. „Untersuchungen von in-vitro-Verfahren zum Nachweis einer Beteiligung von G-Protein-gekoppelten Rezeptorkinasen (GRK) an der Phosphorylierung des Anaphylatoxin-Rezeptors C3aR /“. 2003. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=012969315&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Koleva, Milena [Verfasser]. „De-novo-Induktion von Anaphylatoxin-C5a-Rezeptoren in Hepatocyten der Ratte durch den Entzündungsauslöser Lipopolysaccharid in vivo : Vermittlung durch die Entzündungsmediatoren Interleukin-6 und -1β / vorgelegt von Milena Koleva“. 2001. http://d-nb.info/965256928/34.

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Bälder, Ralf [Verfasser]. „Die Bedeutung der Anaphylatoxine C3a und C5a im Mausmodell der allergischen Atemwegsentzündung / von Ralf Bälder“. 2004. http://d-nb.info/973165596/34.

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Martel, Catherine. „Activation du système du complément dans les syndromes coronariens aigus“. Thèse, 2004. http://hdl.handle.net/1866/15286.

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Crass, Torsten [Verfasser]. „Die Anaphylatoxine C3a und C5a und ihre zellulären Rezeptoren : molekulare Untersuchungen zur Ligand-Rezeptor-Interaktion ; 1. Molekulare Klonierung und Charakterisierung des humanen C3a-Rezeptors, 2. Generierung und Charakterisierung von C3a-Rezeptor-/C5a-Rezeptor-Chimären, 3. Charakterisierung von C-terminalen C5a-Mutanten / von Torsten Crass“. 1999. http://d-nb.info/957116462/34.

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