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Results for “Complement C5”

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PubMed1989

1H nuclear magnetic resonance assignments and secondary structure of porcine C5ades Arg.

Sequence-specific assignments of the 1H nuclear magnetic resonance spectrum of porcine C5ades Arg are described. Assignments were facilitated by comparison of spectra obtained in H2O with partially exchanged spectra obtained in 2H2O. The sequence-specific assignments thus obtained were used to characterized the regular secondary structure in the protein, which is helical in the regions 2 to 11, 16 to 27, 35 to 41 and 45 to 64. The structure is very similar to that of human and bovine C5a.

Amino Acid Sequence↗

PubMed1985

Regulation of monocyte function by complement activation products.

Normal human monocytes, obtained at a mean purity of 60% by Percoll density gradient centrifugation, were found to be chemotactically deactivated to C5a by exposure to low, and biologically significant, concentrations of zymosan-activated serum (ZAS), while retaining their full response to FMLP. C5a was found to be 40X more potent than its metabolite C5adesArg in reducing chemotaxis to activated pooled serum. Conversely, exposure of monocytes to varying concentrations of N-formyl-methionyl-leucyl-phenylalanine (FMLP) decreased chemotaxis to that attractant, though had no effect on chemotaxis to activated serum. Monocytes were also found to actively absorb C5a from solutions of ZAS, rich in C5a. Our data support the concept that monocytes are specifically regulated by C5a and C5adesArg.

Blood↗

PubMed1989

Anaphylatoxin generation in acute pancreatitis.

Fifty-one patients with elevated serum amylase and clinical signs of acute pancreatitis were studied prospectively. The concentrations of anaphylatoxins (C3a and C5a) were measured with a radioimmunoassay and the activity of their inactivator was determined. The pancreatitis was classified as mild, moderate, or severe according to Ranson's 11 signs, appearance of peritoneal fluid, and development of multisystem organ failure (MSOF). Plasma C3a and C5a concentrations were elevated during attacks of acute pancreatitis. Anaphylatoxin levels correlated with the severity of the disease (C3a, P less than 0.001; C5a, P less than 0.05). The highest and most persistent levels were found in the group with MSOF. C3a levels decreased rapidly during recovery. In patients with complications like abscess or pseudocyst, the C3a elevation persisted until adequate treatment was instituted. In this study, no significant changes of the inactivator levels were found, except at discharge when the inactivator level of the severe group was elevated compared to that of the moderate and mild groups (P less than 0.05).

Acute Disease↗

PubMedDate not supplied

Interaction of human beta-endorphin with the terminal SC5b-9 and "preterminal" SC5b-7 and SC5b-8 complexes of human complement.

Human beta-endorphin (beta H-EP) is demonstrated to bind to the "preterminal" SC5b-7 and SC5b-8 complexes and to the terminal SC5b-9 complex of human complement. Detailed binding studies revealed saturability, reversibility and structural specificity of the beta H-EP interaction with high or low affinity non-opiate binding sites on SC5b-7 and SC5b-9 complexes. The high affinity binding sites seem to be located predominantly on C5b, C6 or C7 subunits of the complexes.

Alpha-Globulins↗

PubMed1983

Neutrophil activation as a mechanism of tissue injury.

C5A is capable of causing granulocyte/granulocyte interactions that lead to clumping, vasoocclusion, and the extension of infarctive damage in patients with coronary artery disease. Employing a new rheologic procedure, laser transillumination of thin vascular beds, one directly observes in vivo granulocyte aggregation in the mesentery of the rat. Nonsteroidal antiinflammatory drugs (NSAIDs) were shown to stop granulocyte agglomeration and to limit the extension of experimental myocardial infarcts in the cat. There may be application for NSAIDs for myocardial infarction in humans. NSAIDs block granulocyte aggregation to both a traditional activated complement and a complement activated by cryoglobulins. Patients with severe cryoglobulinemic cutaneous vasculitis who failed on steroids responded to NSAID administration.

Animals↗

PubMed1984

Inflammatory mediators stimulate granulocyte adherence to cultured human endothelial cells.

The factors that regulate the adherence of granulocytes to the endothelium under normal conditions, and in states of inflammatory vascular injury, are largely unknown. We found that treatment of primary, confluent monolayers of human umbilical vein endothelial cells with inflammatory mediators (zymosan-activated plasma, as a source of C5a fragments, and N-formylmethionyl-leucyl-phenylalanine) stimulated granulocyte adherence to the monolayers. The augmented adherence was dose-, time-, and temperature-related and demonstrated kinetics characteristic of the adherence of single cells with increased affinity for monolayer cultures. Adherence stimulated by the inflammatory mediators was not prevented by washing the monolayers after treatment with the mediator. Human albumin diminished both spontaneous and stimulated adherence, although the relative increase in adherence stimulated by the inflammatory mediator was unchanged. Calcium and magnesium were required for stimulated adherence. These data suggest that inflammatory mediators may bind to, or directly alter, human endothelial cells resulting in enhanced granulocyte adherence, and define characteristics of this endothelial cell-granulocyte interaction.

Cell Adhesion↗

PubMed1987