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Journal articles on the topic 'Anaphylatoxin'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Stimler-Gerard, Norma P. "Immunopharmacology of Anaphylatoxin-Induced Bronchoconstrictor Responses." Complement 3, no. 3 (1986): 137–51. http://dx.doi.org/10.1159/000467891.

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12

Hammerschmidt, Dale E. "Clinical Utility of Complement Anaphylatoxin Assays." Complement 3, no. 3 (1986): 166–76. http://dx.doi.org/10.1159/000467893.

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13

Ember, Julia A., Nils L. Johansen, and Tony E. Hugli. "Designing synthetic superagonists of C3a anaphylatoxin." Biochemistry 30, no. 15 (April 16, 1991): 3603–12. http://dx.doi.org/10.1021/bi00229a003.

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14

Barnum, Scott R. "C4a: An Anaphylatoxin in Name Only." Journal of Innate Immunity 7, no. 4 (February 6, 2015): 333–39. http://dx.doi.org/10.1159/000371423.

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15

Akatsu, Hiroyasu, Masayoshi Abe, Takashi Miwa, Hisashi Tateyama, Seiji Maeda, Noriko Okada, Kiyohide Kojima, and Hidechika Okada. "Distribution of Rat C5a Anaphylatoxin Receptor." Microbiology and Immunology 46, no. 12 (December 2002): 863–74. http://dx.doi.org/10.1111/j.1348-0421.2002.tb02774.x.

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16

Nagata, Shoji, Michael Glovsky, and Steven L. Kunkel. "Anaphylatoxin-Induced Neutrophil Chemotaxis and Aggregation." International Archives of Allergy and Immunology 82, no. 1 (1987): 4–9. http://dx.doi.org/10.1159/000234281.

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17

Harada, Tamotsu, Masafumi Sakagami, Mitsuhito Sano, and Toru Matsunaga. "Measurement of Anaphylatoxin Activity During Surgery." Acta Oto-Laryngologica 113, sup501 (January 1993): 88–91. http://dx.doi.org/10.3109/00016489309126223.

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18

Ribeiro, J. M. C., and A. Spielman. "Ixodes dammini: Salivary anaphylatoxin inactivating activity." Experimental Parasitology 62, no. 2 (October 1986): 292–97. http://dx.doi.org/10.1016/0014-4894(86)90034-2.

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19

Jun, Sung Whan, Tae Hoon Kim, Heung Man Lee, Seung Hoon Lee, Woo Joo Kim, Se Jin Park, Yang Soo Kim, and Sang Hag Lee. "Overexpression of the anaphylatoxin receptors, complement anaphylatoxin 3a receptor and complement anaphylatoxin 5a receptor, in the nasal mucosa of patients with mild and severe persistent allergic rhinitis." Journal of Allergy and Clinical Immunology 122, no. 1 (July 2008): 119–25. http://dx.doi.org/10.1016/j.jaci.2008.04.028.

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20

Cannon, Aoife, Danica Lavin, Róisín Byrne, John Reynolds, Jacintha O'Sullivan, and Niamh Lynam-Lennon. "RA10.02: A NOVEL ROLE FOR THE COMPLEMENT CASCADE IN CHEMORADIATION THERAPY RESISTANT OESOPHAGEAL ADENOCARCINOMA." Diseases of the Esophagus 31, Supplement_1 (September 1, 2018): 42. http://dx.doi.org/10.1093/dote/doy089.ra10.02.

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Abstract Background Resistance to chemoradiation therapy (CRT) in oesophageal adenocarcinoma (OAC) is an important clinical challenge. Elucidating underlying mechanisms of treatment resistance is crucial to improving survival rates. Methods OAC tumour biopsies were collected prior to neoadjuvant CRT. Tumour conditioned media was generated by culturing human explants for 24 h. Response to treatment was determined pathologically using the Mandard Grading System. C3, CFB and MCP-1 mRNA expression was assessed by qPCR. Secreted C3, C3a and MCP-1 were measured by ELISA. An isogenic model of radioresistant OAC was established by chronically irradiating OE33 cells with clinically-relevant doses of 2 Gy X-ray radiation. C5aR and C3aR expression was determined by flow cytometry. Results We demonstrate, for the first time, that the central factor of the complement cascade, complement component 3 (C3), is expressed in OAC tumours and is increased in pre-treatment OAC biopsies from patients (n = 13) who have a subsequent poor response to neoadjuvant CRT (P < 0.05). In addition, C3 is secreted from ex vivo human OAC tumour explants (n = 13) and correlates with levels of the monocyte chemoattractant MCP-1 (P < 0.008) and complement factor B (CFB) a component of the alternative pathway of complement activation (P < 0.0001). In vitro, radioresistant OE33 R cells had increased mRNA levels of C3 (P < 0.01), CFB (P < 0.05) and MCP-1 (P < 0.05) compared to radiosensitive OE33 P cells. OEE3 R cells expressed increased levels of secreted C3 and the anaphylatoxin C3a, compared to radiosensitive OE33P cells (both P < 0.001). Furthermore, we demonstrate for the first time that the anaphylatoxin receptor C5aR is expressed by OAC cells, suggesting that OAC cells can respond to complement anaphylatoxins. Conclusion This study highlights, for the first time, a novel role for the complement cascade in the resistance of OAC to CRT and highlights C3 as a novel predictive marker of response to CRT in OAC. Disclosure All authors have declared no conflicts of interest.

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21

Nekrasova, Kseniya A., Alexander M. Ischenko, and Alexander V. Trofimov. "Inhibition of the complement anaphylatoxin activities in the central nervous system disorders." Medical academic journal 21, no. 2 (September 24, 2021): 37–52. http://dx.doi.org/10.17816/maj71315.

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The review is devoted to inhibition of the complement anaphylatoxin activities in diseases of the central nervous system. Here we present epidemiological data on the prevalence of cerebrovascular diseases, in particular, ischemic stroke and craniocerebral trauma. The mechanisms of complement activation and complement-mediated pathology in the central nervous system are considered in detail. Clinical data confirming the role of the complement system in the pathogenesis of stroke and of traumatic brain injury secondary injury are presented. We also summarize the results of in vivo specific activity studies of the complement anaphylatoxin inhibitors using animal models of stroke and traumatic brain injury. Briefly described is the present state of the art in developing drugs that target the effector compounds of the complement cascade.

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22

TERUI, TADASHI, HIDEAKI TAKEMATSU, TAIZO KATO, KYOKO OHKOHCHI, and HACHIRO TAGAMI. "Plasma anaphylatoxin concentrations in inflammatory skin diseases." Tohoku Journal of Experimental Medicine 151, no. 2 (1987): 245–52. http://dx.doi.org/10.1620/tjem.151.245.

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23

Schellenberg, R. R., J. B. Mullen, A. Foster, and M. M. Glovsky. "Anaphylatoxin C3a peptide contracts human pulmonary vasculature." Pulmonary Pharmacology 1, no. 3 (January 1988): 133–38. http://dx.doi.org/10.1016/s0952-0600(88)80011-5.

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24

Das, Dola, Mark A. Barnes, and Laura E. Nagy. "Anaphylatoxin C5a modulates hepatic stellate cell migration." Fibrogenesis & Tissue Repair 7, no. 1 (2014): 9. http://dx.doi.org/10.1186/1755-1536-7-9.

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25

Ember, Julia, Nils Johansen, and Tony Hugli. "Corrections - Designing Synthetic Superagonists of C3a Anaphylatoxin." Biochemistry 30, no. 25 (June 1991): 6350. http://dx.doi.org/10.1021/bi00239a600.

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26

Oppermann, Martin, and Otto Götze. "Inhibition of C5a anaphylatoxin activity in vivo." Shock 7, Supplement (March 1997): 72–73. http://dx.doi.org/10.1097/00024382-199703001-00291.

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27

Gerard, Norma P., and Craig Gerard. "The chemotactic receptor for human C5a anaphylatoxin." Nature 349, no. 6310 (February 1991): 614–17. http://dx.doi.org/10.1038/349614a0.

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28

"New Drug Target in Atherosclerosis: Anaphylatoxin C5a." Asian Journal of Biological Sciences 4, no. 4 (May 1, 2011): 395. http://dx.doi.org/10.3923/ajbs.2011.395.395.

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29

Toth, Matthew J., Leslie Huwyler, William C. Boyar, Albert F. Braunwalder, Donna Yarwood, Joseph Hadala, William O. Haston, Matthew A. Sills, Bruce Seligmann, and Nicholas Galakatos. "The pharmacophore of the human C5a anaphylatoxin." Protein Science 3, no. 8 (August 1994): 1159–68. http://dx.doi.org/10.1002/pro.5560030802.

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30

Soruri, Afsaneh, Ziba Kiafard, Claudia Dettmer, Joachim Riggert, Jörg Köhl, and Jörg Zwirner. "IL-4 Down-Regulates Anaphylatoxin Receptors in Monocytes and Dendritic Cells and Impairs Anaphylatoxin-Induced Migration In Vivo." Journal of Immunology 170, no. 6 (March 15, 2003): 3306–14. http://dx.doi.org/10.4049/jimmunol.170.6.3306.

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31

Koelman, Diederik L. H., Matthijs C. Brouwer, and Diederik van de Beek. "Targeting the complement system in bacterial meningitis." Brain 142, no. 11 (August 2, 2019): 3325–37. http://dx.doi.org/10.1093/brain/awz222.

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Morbidity and mortality in bacterial meningitis are driven by an uncontrolled host inflammatory response. Koelman et al. evaluate the detrimental role of the complement system in spurring this inflammation, and conclude that anaphylatoxin C5a is a promising treatment target in bacterial meningitis.

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32

Abe, Masayoshi, Noriko Satoh, Takehiro Umemura, Akinori Iwasaki, Takayuki Shirakusa, and Takeshi Katsuragi. "Anaphylatoxin C5a potentiates allergic inflammation in human lungs." Molecular Immunology 44, no. 1-3 (January 2007): 147–48. http://dx.doi.org/10.1016/j.molimm.2006.07.007.

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33

Takabayashi, Tsukasa, Soichi Shimizu, Burton D. Clark, Martin Beinborn, John F. Burke, and Jeffrey A. Gelfand. "Interleukin-1 upregulates anaphylatoxin receptors on mononuclear cells." Surgery 135, no. 5 (May 2004): 544–54. http://dx.doi.org/10.1016/j.surg.2003.09.010.

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34

Kourtzelis, Ioannis, Maciej M. Markiewski, Michael Doumas, Stavros Rafail, Konstantinos Kambas, Ioannis Mitroulis, Stelios Panagoutsos, Ploumis Passadakis, Vasilios Vargemezis, and Paola Magotti. "Complement anaphylatoxin C5a contributes to hemodialysis-associated thrombosis." Molecular Immunology 47, no. 13 (August 2010): 2284. http://dx.doi.org/10.1016/j.molimm.2010.05.255.

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35

Gerard, C., and N. P. Gerard. "C5A Anaphylatoxin and Its Seven Transmembrane-Segment Receptor." Annual Review of Immunology 12, no. 1 (April 1994): 775–808. http://dx.doi.org/10.1146/annurev.iy.12.040194.004015.

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36

KRETZSCHMAR, Titus, Martina POHL, Monika CASARETTO, Michael PRZEWOSNY, Wilfried BAUTSCH, Andreas KLOS, Derek SAUNDERS, and Jorg KOHL. "Synthetic peptides as antagonists of the anaphylatoxin C3a." European Journal of Biochemistry 210, no. 1 (November 1992): 185–91. http://dx.doi.org/10.1111/j.1432-1033.1992.tb17407.x.

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37

Li, Rui, Liam G. Coulthard, M. C. L. Wu, Stephen M. Taylor, and Trent M. Woodruff. "C5L2: a controversial receptor of complement anaphylatoxin, C5a." FASEB Journal 27, no. 3 (December 13, 2012): 855–64. http://dx.doi.org/10.1096/fj.12-220509.

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38

del Balzo, U. H., R. Levi, and M. J. Polley. "Cardiac dysfunction caused by purified human C3a anaphylatoxin." Proceedings of the National Academy of Sciences 82, no. 3 (February 1, 1985): 886–90. http://dx.doi.org/10.1073/pnas.82.3.886.

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39

Nemali, Sailasree, Daniel W. Siemsen, Laura K. Nelson, Peggy L. Bunger, Craig L. Faulkner, Pascal Rainard, Katherine A. Gauss, Mark A. Jutila, and Mark T. Quinn. "Molecular analysis of the bovine anaphylatoxin C5a receptor." Journal of Leukocyte Biology 84, no. 2 (May 14, 2008): 537–49. http://dx.doi.org/10.1189/jlb.0208142.

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40

Moskopp*, D., and A. Löcherbach-Zawadzky. "Unusual anaphylatoxin dynamics after head injury - Case report." min - Minimally Invasive Neurosurgery 29, no. 05 (September 1986): 203–5. http://dx.doi.org/10.1055/s-2008-1054161.

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41

Bielecka, Ewa, Carsten Scavenius, Tomasz Kantyka, Monika Jusko, Danuta Mizgalska, Borys Szmigielski, Barbara Potempa, et al. "Peptidyl Arginine Deiminase fromPorphyromonas gingivalisAbolishes Anaphylatoxin C5a Activity." Journal of Biological Chemistry 289, no. 47 (October 16, 2014): 32481–87. http://dx.doi.org/10.1074/jbc.c114.617142.

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42

Cui, Lianxian, Kevin Ferreri, and Tony E. Hugli. "Structural characterization of the C4a anaphylatoxin from rat." Molecular Immunology 25, no. 7 (July 1988): 663–71. http://dx.doi.org/10.1016/0161-5890(88)90101-0.

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43

Kourtzelis, Ioannis, Maciej M. Markiewski, Michael Doumas, Stavros Rafail, Konstantinos Kambas, Ioannis Mitroulis, Stelios Panagoutsos, et al. "Complement anaphylatoxin C5a contributes to hemodialysis-associated thrombosis." Blood 116, no. 4 (July 29, 2010): 631–39. http://dx.doi.org/10.1182/blood-2010-01-264051.

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Abstract Thrombosis is a common complication of end-stage renal disease, particularly in patients on hemodialysis. Although substantial progress has been made in preventing thrombotic complications in various other groups of patients, the mechanisms of thrombosis during hemodialysis require clarification. In this report, we demonstrate that complement activation triggered by hemodialysis biomaterials, and the subsequent generation of the complement anaphylatoxin C5a, results in the expression of functionally active tissue factor (TF) in peripheral blood neutrophils. Because TF is a key initiator of coagulation in vivo, we postulate that the recurring complement activation that occurs during long-term hemodialysis contributes to thrombosis in dialyzed end-stage renal disease patients. Furthermore, we found that complement contributed to the induction of granulocyte colony-stimulating factor, which has been implicated in the pathogenesis of thrombosis in patients treated with the recombinant form of this molecule. Importantly, the inhibition of complement activation attenuated the TF expression and granulocyte colony-stimulating factor induction in blood passing through a hemodialysis circuit, suggesting that the complement system could become a new therapeutic target for preventing thrombosis in patients with chronic renal failure who are maintained on hemodialysis.

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44

Ward, C. A., D. McCullough, and W. D. Fraser. "Relation between complement activation and susceptibility to decompression sickness." Journal of Applied Physiology 62, no. 3 (March 1, 1987): 1160–66. http://dx.doi.org/10.1152/jappl.1987.62.3.1160.

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The consequences of complement activation and the symptoms of decompression sickness are similar. Consequently, the relation between the sensitivity of individuals to complement activation by air bubbles and their susceptibility to decompression sickness has been examined. Plasma samples from 34 individuals were incubated with air bubbles, and the concentration of the fluid phase metabolites of complement activation C3a, C4a, and C5a were measured with radioimmunoassays. It was found that both the anaphylatoxins C3a and C5a were produced by the presence of air bubbles but that the anaphylatoxin C4a was not. This finding indicates that air bubbles activate the complement system by the alternate pathway. One group of individuals was found to be particularly sensitive to complement activation by this pathway. They produced 3.3 times more C3a and 5.3 times more C5a in their plasma samples incubated with air bubbles as did the other group. Sixteen individuals were subjected to a series of pressure profiles that were severe enough to produce bubbles in their circulatory system that could be detected by Doppler ultrasonic monitoring. The group of individuals that had been identified as being more sensitive to complement activation by the alternate pathway was also found to be more susceptible to decompression sickness.

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45

Schmidt, Carolin, Sabrina Weißmüller, Fabian Bohländer, Matthias Germer, Martin König, Alexander Staus, Andrea Wartenberg-Demand, Corina C. Heinz, and Jörg Schüttrumpf. "The Dual Role of a Polyvalent IgM/IgA-Enriched Immunoglobulin Preparation in Activating and Inhibiting the Complement System." Biomedicines 9, no. 7 (July 14, 2021): 817. http://dx.doi.org/10.3390/biomedicines9070817.

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Activation of the complement system is important for efficient clearance of a wide variety of pathogens via opsonophagocytosis, or by direct lysis via complement-dependent cytotoxicity (CDC). However, in severe infections dysregulation of the complement system contributes to hyperinflammation. The influence of the novel IgM/IgA-enriched immunoglobulin preparation trimodulin on the complement pathway was investigated in in vitro opsonophagocytosis, binding and CDC assays. Immunoglobulin levels before and after trimodulin treatment were placed in relation to complement assessments in humans. In vitro, trimodulin activates complement and induces opsonophagocytosis, but also interacts with opsonins C3b, C4b and anaphylatoxin C5a in a concentration-dependent manner. This was not observed for standard intravenous IgG preparation (IVIg). Accordingly, trimodulin, but not IVIg, inhibited the downstream CDC pathway and target cell lysis. If applied at a similar concentration range in healthy subjects, trimodulin treatment resulted in C3 and C4 consumption in a concentration-dependent manner, which was extended in patients with severe community-acquired pneumonia. Complement consumption is found to be dependent on underlying immunoglobulin levels, particularly IgM, pinpointing their regulative function in humans. IgM/IgA provide a balancing effect on the complement system. Trimodulin may enhance phagocytosis and opsonophagocytosis in patients with severe infections and prevent excessive pathogen lysis and release of harmful anaphylatoxins.

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46

Holland, M. Claire H., and John D. Lambris. "A Functional C5a Anaphylatoxin Receptor in a Teleost Species." Journal of Immunology 172, no. 1 (December 19, 2003): 349–55. http://dx.doi.org/10.4049/jimmunol.172.1.349.

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47

Harada, Tamotsu, Mitsuhito Sano, and Toru Matsunaga. "Cochlear Damage Caused by Anaphylatoxin in the Tympanic Cavity." Equilibrium Research 49, Suppl-6 (1990): 31–35. http://dx.doi.org/10.3757/jser.49.suppl-6_31.

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Shiba, M., K. Tadokoro, K. Tokunaga, and T. Juji. "Histamine, cytokine and anaphylatoxin levels in stored platelet concentrates." Journal of the Japan Society of Blood Transfusion 40, no. 5 (1994): 716–20. http://dx.doi.org/10.3925/jjtc1958.40.716.

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Wetsel, Rick A. "Structure, function and cellular expression of complement anaphylatoxin receptors." Current Opinion in Immunology 7, no. 1 (February 1995): 48–53. http://dx.doi.org/10.1016/0952-7915(95)80028-x.

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Okada, Noriko, Suzuka Asai, Aya Hotta, Noriko Miura, Naohito Ohno, Imre Farkas, Lewis Hau, William Campbell, and Hidechika Okada. "An inhibitory complementary peptide of C5a anaphylatoxin restricts inflammation." Molecular Immunology 44, no. 1-3 (January 2007): 222. http://dx.doi.org/10.1016/j.molimm.2006.07.175.

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