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PubMed1992

[Inhibition of Cls activity by methylprednisolone].

From a clinical study it was found that serum ClINH activity increased 6 hours after methylprednisolone (MP) pulse therapy in all the patients we studied with connective tissue diseases. Furthermore plasma ClINH-Cls complex decreased after pulse therapy. These phenomena lead us to investigate the effect of MP on Cls. 1) When a constant amount of Cls (8 micrograms/ml) was incubated with several concentrations of MP (2-50 mg/ml), the Cls activity of consuming C4 hemolysis was inhibited by MP in a dose-dependent manner. 2) MP inhibited consumption of C2 as well as C4 by Cls in a dose-dependent manner, even when MP had been removed by dialysis following incubation with Cls. These experimental data suggested that the trace amounts of Cls generated by immune complexes could be inhibited by long circulation of MP even at low concentrations in vivo, and resulted in a decrease of ClINH consumption and ClINH-Cls complex formation. These results indicated that the inhibition of Cls activity is one of the most important mechanisms in the process of the anti-inflammatory effect of MP in vivo.

Complement C1 Inactivator Proteins↗
PubMed1991

Human recombinant macrophage colony-stimulating factor (M-CSF) increases Cl-esterase inhibitor (Cl-INH) synthesis by human monocytes.

The ability of macrophage colony-stimulating factor (M-CSF) to influence production of complement proteins by cultured human monocytes was studied. Three-day-old cultures of human monocytes were treated with 250-1000 U/ml recombinant human M-CSF (Cetus Corporation, Emeryville, CA). After 3 days the M-CSF containing medium was replaced by the same medium without M-CSF, and the cells were cultured for 3 more days. Samples taken at the removal of M-CSF and 3 days later were tested for the concentration of factor B and Cl-esterase inhibitor (Cl-INH) using ELISA methods, and C2 by using an immunohaemolytic assay. M-CSF induced a marked dose-dependent increase in the synthesis of Cl-INH, but did not significantly change Bf and C2 production. The findings suggest that M-CSF is able to influence selectively the complement protein-producing ability of cultured human monocytes.

Cells, Cultured↗
PubMed1978

Activation of the kallikrein system in hyperbetalipoproteinemia.

In 30 patients with hyperlipoproteinemia (19 type II and 11 type IV), the role of the intrinsic coagulation pathway was evaluated by assays of preK, Kl's, and Hageman factor (factor XII). Analysis of the plasma of type II patients suggested activation of the intrinsic pathway characterized by a 40% decrease in preK (p less than 0.01) and a 50% decrease Kl (p less than 0.01); in contrast, analysis of the plasma of type IV patients showed no activation of the intrinsic pathway. In type II patients C-1INH was present in normal concentrations as measured by immunochemical techniques. The findings of normal levels of C-1INH by immunoassay, in association with altered electrophoretic mobility, are suggestive of formation of a kallikrein-C-1INH complex in vivo.

Blood Coagulation↗
PubMed1989

C1q interactions with cell surface receptors.

The defense mechanisms initiated by the human body against foreign entities such as invading pathogenic bacteria and viruses involve intricate sequences of interactions between cells and macromolecules of the immune system. The complement system is a multienzymatic cascade which upon activation by either of two distinct mechanisms leads to the assembly of a common membranolytic complex of proteins, as well as the generation of protein fragments which mediate inflammation and enhance phagocytosis. It has now been clearly established that C1q, the initial component of the classical complement pathway, interacts in a specific manner with several immunologically important cell types, including B cells, monocytes, macrophages and polymorphonuclear leukocytes. Thus it has an uncommon potential for participating in a cellular-humoral immune network. Furthermore, since it binds both antibody-antigen complexes and other non-antibody containing activators of the classical complement pathway, C1q could provide a very efficient, direct means of modulating the immune response especially during early stages of disease when little or no antibody is present. In vitro, C1q has been shown to be capable of stimulating a number of potentially useful immune cell functions including the enhancement of phagocytosis, stimulation of oxygen radical generation and stimulation of immunoglobulin secretion. In addition, individuals which are genetically C1q-deficient develop immune-complex related disease (primarily lupus-like) and/or have severe bouts with infection. Thus, while the structure and mode of action of the cell surface C1q receptor(s) are currently unclear, it is clear that C1q has multiple significant effects on cellular immune function.

B-Lymphocytes↗
PubMed1977

An investigation of the complement system in patients with periodic disease (results from 29 cases).

The complement system was investigated in 29 patients suffering from authentic periodic disease. A statistically significant increase in C4, also in total complement and C3 could be demonstrated. It is possible that the increase in C4 was due to the macrophages which are always present in the infiltrates of periodic disease. This biological observation is of clear practical importance for the diagnosis of the condition both before and after colchicine therapy.

Complement C1 Inactivator Proteins↗
PubMed1978

Inhibition of the classical and alternative pathways by amino acids and their derivatives.

Effects of various aminoacids and their derivatives on the classical pathway and alternative pathway of the complement were studied. Leupeptin, acetyl-leucyl-leucyl-arginal, inhibited CH50 and Cl-esterase, but did not inhibit the alternative pathway. When aminoacids of carbon chains of the order of seven were used, arginine and lysine had stronger effects than trans-aminomethyl cyclohexane carboxylic acid (t-AMCHA), cis-aminomethyl cyclohexane carboxylic acid (cis-AMCHA) and epsilon aminocaproic acid (EACA). SH-compounds, cysteine, homocysteine and glutathione, had the strongest inhibitory effects among these aminoacids on both classical and alternative pathways. When effects on Cl esterase were compared, arginine, lysine, t-AMCHA, cis-AMCHA and EACA had weak inhibition while SH-compounds showed strong inhibition. Poly-L-lysine, which had extremely strong inhibition of CH50, had no inhibition of Cl esterase. The inhibitory effects of antifibrinolytic agents, EACA and t-AMCHA, were weak but when effects on early parts of the classical pathway, C(1,4,2)H50 were tested, some inhibitory activities were recognized. Thus inhibitory effects of these agents were due to their activities on the early parts of the classical pathway.

Amino Acids↗