The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Chemical Compound Review

AC1O4WLL     propylN-[(2S,3R)-3-hydroxy-3- [5-[[4-(2H...

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of C3a

  • However, many features of bronchial asthma, such as smooth muscle contraction, mucus secretion and recruitment of inflammatory cells, are consistent with the actions of complement anaphylatoxins, in particular C3a and C5a [1].
  • It seems likely that C3a generated in the course of pulmonary inflammation might contribute to the mucus secretion associated with pulmonary infections [2].
  • The anaphylatoxins complement component 3a and 5a (C3a and C5a, respectively) are classically seen as proinflammatory mediators of allergic asthma that recruit inflammatory cells, induce edema, and cause bronchoconstriction [3].
  • The generation of the anaphylatoxin C3a was measured after a wasp-sting challenge in eight patients with previous anaphylactic reactions to wasp stings [4].
  • Recently, several investigators have implicated the complement anaphylatoxins C3a and C5a as potential effectors in Type 1 hypersensitivity reactions, including urticaria, rhinitis and asthma [5].

Psychiatry related information on C3a


High impact information on C3a


Chemical compound and disease context of C3a


Biological context of C3a


Anatomical context of C3a

  • C5a desArg (but not C3a desArg) induced a comparable increase in Mo1 expression on normal granulocytes in vitro at concentrations similar to those measured in vivo [8].
  • Single-cell calcium measurements in HMC-1 human mast cells showed that a rise in intracellular calcium caused by C3a and C5a was inhibited in a concentration-dependent manner by IVIG, F(ab)2-IVIG and irrelevant human monoclonal antibody [18].
  • C3a activates eosinophils in the presence of anti-C5aR antibody at concentrations that fully block C5a activation [15].
  • In contrast, C3a had no effect on antigen- or mitogen-induced B or T cell proliferative responses [17].
  • Recent reports that C3a activates both basophils and eosinophils prompted us to reinvestigate the effects of C3a stimulation on eosinophils [15].

Associations of C3a with other chemical compounds

  • Mice with dual C3 and C5 deficiency had a more exacerbated phenotype that was reversed by combined C3a and C5a reconstitution [19].
  • The serum carboxypeptidase inhibitor 2-mercaptomethyl-5-guanodinopentanoic acid, which prevents cleavage of the terminal arginine that would produce C3ades Arg-77, allowed us to assay the effects of C3a on in vitro immune response systems where serum is required [17].
  • The generation of LIF activity was inhibited by 50% by 10(-8) M C3a or C3a(70-77) with PHA or Con A as the stimulus, whereas a more than 10-fold higher concentration of C3a(70-77) than C3a was required to achieve the same level of suppression with SK-SD as the stimulus [20].
  • Purified human C3a and synthetic COOH-terminal peptides of C3a, i.e., a pentapeptide, Leu-Gly-Leu-Ala-Arg (5R), and an octapeptide, Ala-Ala-Ala-Leu-Gly-Leu-Ala-Arg (8R) induced histamine release from human basophil granulocytes [21].
  • Flow cytometric measurement of H2O2 by dihydrorhodamine-123 labeling of anti-CD16-stained PMN showed that predominantly neutrophilic PMN are responsible for the C3a-induced activation of the respiratory burst [14].

Gene context of C3a

  • The proinflammatory mediators C3a and C5a are essential for liver regeneration [19].
  • Twenty-two adult patients aged 41 to 81 years undergoing coronary revascularization were studied for measurements of C3a, C5a, IL-1, IL-8, and OH(.). Blood was collected before surgery, after CPB, and at 24, 48, and 72 hours [22].
  • We report that normal human CD34(+) cells and lineage-differentiated hematopoietic progenitors express the complement anaphylatoxin C3a receptor (C3aR) and respond to C3a [23].
  • Functional receptor for C3a anaphylatoxin is expressed by normal hematopoietic stem/progenitor cells, and C3a enhances their homing-related responses to SDF-1 [23].
  • Thus, similar to NAP-1/IL-8 and C3a, PAF efficiently stimulates mediator release in hGF-primed basophils only [24].

Analytical, diagnostic and therapeutic context of C3a


  1. A role for the C3a anaphylatoxin receptor in the effector phase of asthma. Humbles, A.A., Lu, B., Nilsson, C.A., Lilly, C., Israel, E., Fujiwara, Y., Gerard, N.P., Gerard, C. Nature (2000) [Pubmed]
  2. Anaphylatoxin C3a enhances mucous glycoprotein release from human airways in vitro. Marom, Z., Shelhamer, J., Berger, M., Frank, M., Kaliner, M. J. Exp. Med. (1985) [Pubmed]
  3. An unexpected role for the anaphylatoxin C5a receptor in allergic sensitization. Lambrecht, B.N. J. Clin. Invest. (2006) [Pubmed]
  4. Preliminary report: complement activation in wasp-sting anaphylaxis. van der Linden, P.W., Hack, C.E., Kerckhaert, J.A., Struyvenberg, A., van der Zwan, J.C. Lancet (1990) [Pubmed]
  5. Complement in allergy and asthma. Gerard, N.P., Gerard, C. Curr. Opin. Immunol. (2002) [Pubmed]
  6. Cerebrospinal fluid C3a increases with age, but does not increase further in Alzheimer's disease. Loeffler, D.A., Brickman, C.M., Juneau, P.L., Perry, M.F., Pomara, N., Lewitt, P.A. Neurobiol. Aging (1997) [Pubmed]
  7. Anti-analgesic and anti-amnesic effect of complement C3a. Jinsmaa, Y., Takahashi, M., Takahashi, M., Yoshikawa, M. Life Sci. (2000) [Pubmed]
  8. Increased expression of an adhesion-promoting surface glycoprotein in the granulocytopenia of hemodialysis. Arnaout, M.A., Hakim, R.M., Todd, R.F., Dana, N., Colten, H.R. N. Engl. J. Med. (1985) [Pubmed]
  9. Complement activation during cardiopulmonary bypass: evidence for generation of C3a and C5a anaphylatoxins. Chenoweth, D.E., Cooper, S.W., Hugli, T.E., Stewart, R.W., Blackstone, E.H., Kirklin, J.W. N. Engl. J. Med. (1981) [Pubmed]
  10. Inability of the C3a anaphylatoxin to promote cellular lysis. Goodman, M.G., Weigle, W.O., Hugli, T.E. Nature (1980) [Pubmed]
  11. Complement anaphylatoxin receptors on neurons: new tricks for old receptors? Nataf, S., Stahel, P.F., Davoust, N., Barnum, S.R. Trends Neurosci. (1999) [Pubmed]
  12. Cardiac dysfunction caused by purified human C3a anaphylatoxin. del Balzo, U.H., Levi, R., Polley, M.J. Proc. Natl. Acad. Sci. U.S.A. (1985) [Pubmed]
  13. Evaluation of thromboxane production and complement activation during myocardial ischemia in patients with angina pectoris. Montalescot, G., Drobinski, G., Maclouf, J., Maillet, F., Salloum, J., Ankri, A., Kazatchkine, M., Eugène, L., Thomas, D., Grosgogeat, Y. Circulation (1991) [Pubmed]
  14. C3a activates the respiratory burst in human polymorphonuclear neutrophilic leukocytes via pertussis toxin-sensitive G-proteins. Elsner, J., Oppermann, M., Czech, W., Kapp, A. Blood (1994) [Pubmed]
  15. C3a is a chemotaxin for human eosinophils but not for neutrophils. I. C3a stimulation of neutrophils is secondary to eosinophil activation. Daffern, P.J., Pfeifer, P.H., Ember, J.A., Hugli, T.E. J. Exp. Med. (1995) [Pubmed]
  16. Human platelet activation by C3a and C3a des-arg. Polley, M.J., Nachman, R.L. J. Exp. Med. (1983) [Pubmed]
  17. Anaphylatoxin-mediated regulation of the immune response. I. C3a-mediated suppression of human and murine humoral immune responses. Morgan, E.L., Weigle, W.O., Hugli, T.E. J. Exp. Med. (1982) [Pubmed]
  18. F(ab)'2-mediated neutralization of C3a and C5a anaphylatoxins: a novel effector function of immunoglobulins. Basta, M., Van Goor, F., Luccioli, S., Billings, E.M., Vortmeyer, A.O., Baranyi, L., Szebeni, J., Alving, C.R., Carroll, M.C., Berkower, I., Stojilkovic, S.S., Metcalfe, D.D. Nat. Med. (2003) [Pubmed]
  19. The proinflammatory mediators C3a and C5a are essential for liver regeneration. Strey, C.W., Markiewski, M., Mastellos, D., Tudoran, R., Spruce, L.A., Greenbaum, L.E., Lambris, J.D. J. Exp. Med. (2003) [Pubmed]
  20. Modulation of human lymphocyte function by C3a and C3a(70-77). Payan, D.G., Trentham, D.E., Goetzl, E.J. J. Exp. Med. (1982) [Pubmed]
  21. Anaphylatoxin-induced histamine release with human leukocytes: studies of C3a leukocyte binding and histamine release. Glovsky, M.M., Hugli, T.E., Ishizaka, T., Lichtenstein, L.M., Erickson, B.W. J. Clin. Invest. (1979) [Pubmed]
  22. Induction of interleukin-8 expression during cardiopulmonary bypass. Kalfin, R.E., Engelman, R.M., Rousou, J.A., Flack, J.E., Deaton, D.W., Kreutzer, D.L., Das, D.K. Circulation (1993) [Pubmed]
  23. Functional receptor for C3a anaphylatoxin is expressed by normal hematopoietic stem/progenitor cells, and C3a enhances their homing-related responses to SDF-1. Reca, R., Mastellos, D., Majka, M., Marquez, L., Ratajczak, J., Franchini, S., Glodek, A., Honczarenko, M., Spruce, L.A., Janowska-Wieczorek, A., Lambris, J.D., Ratajczak, M.Z. Blood (2003) [Pubmed]
  24. Platelet-activating factor induces mediator release by human basophils primed with IL-3, granulocyte-macrophage colony-stimulating factor, or IL-5. Brunner, T., de Weck, A.L., Dahinden, C.A. J. Immunol. (1991) [Pubmed]
  25. The anaphylatoxin C3a downregulates the Th2 response to epicutaneously introduced antigen. Kawamoto, S., Yalcindag, A., Laouini, D., Brodeur, S., Bryce, P., Lu, B., Humbles, A.A., Oettgen, H., Gerard, C., Geha, R.S. J. Clin. Invest. (2004) [Pubmed]
  26. C4a: the third anaphylatoxin of the human complement system. Gorski, J.P., Hugli, T.E., Müller-Eberhard, H.J. Proc. Natl. Acad. Sci. U.S.A. (1979) [Pubmed]
  27. Activation of complement and kinin systems after thrombolytic therapy in patients with acute myocardial infarction. A comparison between streptokinase and recombinant tissue-type plasminogen activator. Agostoni, A., Gardinali, M., Frangi, D., Cafaro, C., Conciato, L., Sponzilli, C., Salvioni, A., Cugno, M., Cicardi, M. Circulation (1994) [Pubmed]
  28. Influence of temperature on neutrophil trafficking during clinical cardiopulmonary bypass. Menasché, P., Peynet, J., Haeffner-Cavaillon, N., Carreno, M.P., de Chaumaray, T., Dillisse, V., Faris, B., Piwnica, A., Bloch, G., Tedgui, A. Circulation (1995) [Pubmed]
WikiGenes - Universities