Measurement of the chemotactic complement fragment C5a in rheumatoid synovial fluids by radioimmunoassay: role of C5a in the acute inflammatory phase.

Evidence suggests that complement is activated in rheumatoid joints. A sensitive radioimmunoassay for the activation fragment of C5, C5a, which is a potent chemoattractant for neutrophils, was therefore developed. A mean C5a concentration in 22 rheumatoid joint fluids of about 2.5 x 10(-9) mol/l was found. This concentration of C5a is sufficient to induce two of the characteristic features of the acute inflammatory phases of rheumatoid arthritis: neutrophil accumulation and microvascular plasma protein leakage. In animal models it has been shown that C5a is a potent inducer of inflammatory oedema by a neutrophil dependent mechanism. A striking feature of the acute inflammatory phases of rheumatoid arthritis is the appearance of high numbers of neutrophils in the synovial fluid. It is suggested that C5a might have a role in mediating neutrophil accumulation and, as a consequence, may be important in acute joint swelling and pain.

[1]  T. Williams,et al.  Evidence that neutrophil accumulation induced by interleukin‐1 requires both local protein biosynthesis and neutrophil CD18 antigen expression in vivo , 1988, British journal of pharmacology.

[2]  K. Yancey,et al.  A direct in vivo comparison of the inflammatory properties of human C5a and C5a des Arg in human skin. , 1988, Journal of immunology.

[3]  K. Yancey.  Biological properties of human C5a: selected in vitro and in vivo studies. , 1988, Clinical and experimental immunology.

[4]  M. Walport,et al.  Monoclonal rheumatoid factor-IgG immune complexes. Poor fixation of opsonic C4 and C3 despite efficient complement activation. , 1988, Arthritis and rheumatism.

[5]  P. Jose.  Complement-derived peptide mediators of inflammation. , 1987, British medical bulletin.

[6]  L. Williamson,et al.  Neutrophils are involved in the increased vascular permeability produced by activated complement in man , 1986, British journal of haematology.

[7]  A. Kaplan,et al.  Characterization and functional studies of rheumatoid synovial mast cells. Activation by secretagogues, anti-IgE, and a histamine-releasing lymphokine. , 1986, Arthritis and rheumatism.

[8]  O. Mellbye,et al.  Complement activation in rheumatoid arthritis evaluated by C3dg and the terminal complement complex. , 1986, Arthritis and rheumatism.

[9]  S. Ruddy,et al.  Elevated C3 anaphylatoxin levels in synovial fluids from patients with rheumatoid arthritis. , 1985, Arthritis and rheumatism.

[10]  J. Solomkin,et al.  Complement activation and clearance in acute illness and injury: evidence for C5a as a cell-directed mediator of the adult respiratory distress syndrome in man. , 1985, Surgery.

[11]  K. Yancey,et al.  Studies of human C5a as a mediator of inflammation in normal human skin. , 1985, The Journal of clinical investigation.

[12]  T. Hugli,et al.  Radioimmunoassay for anaphylatoxins: a sensitive method for determining complement activation products in biological fluids. , 1984, Analytical biochemistry.

[13]  M. Forrest,et al.  Detection of the complement fragment C5a in inflammatory exudates from the rabbit peritoneal cavity using radioimmunoassay , 1983, The Journal of experimental medicine.

[14]  E. Becker.  Chemotactic factors of inflammation , 1983 .

[15]  C. Page,et al.  Chemotactic factors of inflammation , 1983 .

[16]  J F Fries,et al.  The 1982 revised criteria for the classification of systemic lupus erythematosus. , 1982, Arthritis and rheumatism.

[17]  R. Maini,et al.  Measurement of the complement C3 breakdown product C3d by rocket immunoelectrophoresis. , 1982, Journal of immunological methods.

[18]  T. Williams.  Increased Vascular Permeability Following Interaction between Polymorphonuclear Neutrophils and Vascular Endothelial Cells , 1982 .

[19]  M. Forrest,et al.  Human C5a des Arg increases vascular permeability. , 1981, Journal of immunology.

[20]  E. Blackstone,et al.  Complement activation during cardiopulmonary bypass: evidence for generation of C3a and C5a anaphylatoxins. , 1981, The New England journal of medicine.

[21]  T. Williams,et al.  Control of vascular permeability by polymorphonuclear leukocytes in inflammation , 1981, Nature.

[22]  T. Williams,et al.  Mediation of increased vascular permeability after complement activation. Histamine-independent action of rabbit C5a , 1981, The Journal of experimental medicine.

[23]  H. Movat,et al.  Enhanced vascular permeability and haemorrhage-inducing activity of rabbit C5ades arg: probable role of polymorphonuclear leucocyte lysosomes. , 1980, Clinical and experimental immunology.

[24]  K. Whaley,et al.  Alternative pathway complement activation in rheumatoid arthritis. , 1980, The Journal of rheumatology.

[25]  H. Hedberg.  Studies on the depressed hemolytic complement activity of synovial fluid in adult rheumatoid arthritis. , 1980, Scandinavian journal of rheumatology.

[26]  T. Hugli,et al.  Primary structural analysis of the polypeptide portion of human C5a anaphylatoxin. Polypeptide sequence determination and assignment of the oligosaccharide attachment site in C5a. , 1978, The Journal of biological chemistry.

[27]  T. Hugli,et al.  Demonstration of specific C5a receptor on intact human polymorphonuclear leukocytes. , 1978, Proceedings of the National Academy of Sciences of the United States of America.

[28]  H. Müller-Eberhard,et al.  Anaphylatoxins: C3a and C5a. , 1978, Advances in immunology.

[29]  R. Zubler,et al.  Circulating complement breakdown products in patients with rheumatoid arthritis. Correlation between plasma C3d, circulating immune complexes, and clinical activity. , 1977, The Journal of clinical investigation.

[30]  P. Ward.  COMPLEMENT‐DEPENDENT PHLOGISTIC FACTORS IN RHEUMATOID SYNOVIAL FLUIDS * , 1975, Annals of the New York Academy of Sciences.

[31]  R. Snyderman,et al.  BIOLOGICAL ACTIVITY OF COMPLEMENT IN VIVO , 1971, The Journal of experimental medicine.

[32]  P. Ward,et al.  Complement-derived leukotactic factors in inflammatory synovial fluids of humans. , 1971, The Journal of clinical investigation.

[33]  S. Ruddy,et al.  The complement system in rheumatoid synovitis. I. An analysis of complement component activities in rheumatoid synovial fluids. , 1970, Arthritis and rheumatism.

[34]  R. Winchester,et al.  Gamma globulin complexes in synovial fluids of patients with rheumatoid arthritis. Partial characterization and relationship to lowered complement levels. , 1970, Clinical and experimental immunology.

[35]  N. Zvaifler,et al.  HEMOLYTIC COMPLEMENT IN SYNOVIAL FLUID. , 1964, The Journal of clinical investigation.

[36]  G. A. Bennett,et al.  1958 REVISION of diagnostic criteria for rheumatoid arthritis. , 1959, Arthritis and rheumatism.

[37]  M. Ropes.  DIAGNOSTIC criteria for rheumatoid arthritis: 1958 revision by a committee of the American Rheumatism Association. , 1959, Annals of the rheumatic diseases.

[38]  J. Humphrey.  The mechanism of Arthus reactions. I. The role of polymorphonuclear leucocytes and other factors in reversed passive Arthus reactions in rabbits. , 1955, British journal of experimental pathology.