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PubMed1984

Magnitude of bacteremia and complement activation during Neisseria meningitidis infection: study of two co-primary cases with different clinical presentations.

Two co-primary cases of schoolchildren with acute meningococcal disease due to infection with Neisseria meningitidis serogroup B are described. The first patient presented with septic shock and purpura fulminans, bacteremia greater than 10(5) organisms/ml blood, low C3 and factor B levels and an elevated level of C3d. The second patient had meningitis, negative blood cultures, normal levels of serum complement components but more than 10(4) organisms/ml in CSF. A comparison of the quantitative bacteriology data and complement profiles for these patients suggests that the degree of activation of complement during meningococcemia is directly related to the number of organisms in the blood. This association may determine the different clinical syndromes.

Adolescent↗
PubMed1992

Biochemical analysis of Entamoeba histolytica HM1 strain resistant to complement lysis.

In this study, quantitation of several hydrolases and analysis of electrophoretic patterns of E. histolytica HM1 axenic strain periodically exposed to lytic-human serum (lytic-HS), heat-inactivated human (HI-HS) or bovine (HI-BS) sera were performed. The N-acetylglucosaminidase (NAGAse) levels increased in amebas resistant to complement. The acid phosphatase (AP) and proteolytic activity (PA) levels did not vary significantly in all groups of treated amebas, as compared with amebas from axenic cultures. Moreover, amebas exposed to either HI-HS or lytic-HS sera showed a discrete quantitative increase as compared with HI-BS group, in some peptides with a M(r) between 116 and 45 kDa. These results indicate that, besides resistance to complement lysis, exposure of E. histolytica to lytic-HS induces an augmentation in NAGAse levels.

Acetylglucosaminidase↗
PubMedDate not supplied

[A method of evaluating the degree of activation of the complement system in patients during hemodialysis].

A quantitative criterion of the activation of the patient's complement during hemodialysis has been worked out on the basis of the proposed mathematical model. It has been shown that the activation of the complement system observed during hemodialysis and the negative clinical effects (leukopenia, hypoxia) accompanying it depend both on the membrane properties and the patient's individual response. A possibility has been revealed of using the above criterion for the individual choice of hemodialytic membranes in order to reduce the negative clinical effects connected with the activation of the complement system.

Complement Activation↗
PubMed1979

The quantitation of cell surface antigens by antibody-complement mediated cytotoxicity: application to murine leukemia virus-infected mouse cells.

51Cr-antibody-complement mediated cytotoxicity (ACC) can be used to quantify nanogram amounts of cell surface antigens. When pure antigen is available for calibration, inhibition of ACC by known amounts of antigen and by whole cells yields an estimate of the number of antigenic equivalents per cell. ACC is more suitable for this purpose than radioimmunoprecipitation assay. By ACC the number of antigenic equivalents of the oncornaviral proteins gp70 and p30 has been determined on the surface of various cells infected with Rauscher and Gross murine leukemia viruses.

AKR murine leukemia virus↗
PubMed1981

Quantitation and stability of the fifth component of complement (C5) in bronchoalveolar lavage fluids obtained from non-human primates.

The functional activity and antigenic expression of the fifth component of complement (C5) in concentrated bronchoalveolar lavage fluids (BALF) and serum samples obtained from 13 nonsmoking and 13 smoking baboons was quantified by specific hemolytic titration and radioimmunoassays. The number of C5H505 units per milligram of albumin in BALF obtained from nonsmoking and smoking baboons indicated a nearly 2-fold increase in C5 hemolytic activity in lavage fluids as compared to matched serum samples. No significant differences (p greater than 0.05) in C5 hemolytic or antigenic (radioimmunoassay) expression were evident between BALF samples obtained from nonsmoking and smoking baboons. C5 stability in BALF was indicated by the highly significant correlation (p less than 0.005) between C5 hemolytic activity and antigenic expression. The absence of C5-cleaving enzymes in BALF was verified by incubation of 125I-C5 with these fluids, followed by SDS5 polyacrylamide slab gel and autoradiographic analyses. These results demonstrated the presence and stability of substantial quantities of functionally active C5 in the secretions of primate lungs, which represents a readily available source of phlogistic fragments for the initiation of pulmonary inflammation.

Animals↗
PubMed1975

Quantitative comparison of techniques used to measure complement-mediated cytotoxicity of nucleated cells.

?The cytotoxicity of nucleated cells by specific antibody and complement can be guantitated in vitro by several methods. Trypan blue exclusion, 51-Cr release, inhibition of uptake of 3-H-thymidine, and inhibition of colony formation are the four assays that we used to guantitatively compare the C-mediated cytotoxicity of Chinese hamster lung (CHL) cells. CHL cells were sensitized with either guinea pig or rabbit anti-CHL antisera, and exposed to guinea pig, human, or rabbit C. We found that the relative activities of the antibodies and the complements were not dependent on the method of measurement of cytotoxicity, i.e., a given pair of antiserum-complement were not dependent on the method of measurement of cytotoxicity, i.e., a given antiserum-complement titer, regardless of the assay used to measure cytotoxicity. However, the titers of the different antibody-complement pairs differed from each other.

Animals↗
PubMed1990

Quantitative analysis of membrane cofactor protein (MCP) of complement. High expression of MCP on human leukemia cell lines, which is down-regulated during cell differentiation.

Membrane cofactor protein (MCP) is a cell-associated regulatory molecule for C system with C3b/C4b binding and factor I-dependent cofactor activity. mAb were raised against MCP and amounts and distribution examined on normal human cells and cell lines. The mean quantity of MCP was 3000 to 7000 copies/cell in normal blood cells, except for E which have no MCP. Of note, PMN did not fully reveal all MCP sites until incubated for greater than 30 min at 37 degrees C. In most tumor cell lines, except for B cell lineages, expression of MCP increased by 2- to 8-fold in comparison with the normal cell counterparts. Strikingly, recombinant granulocyte CSF treatment of myeloid cell lines and hemin treatment of an erythroblastoid cell line, K562, led to a decrease of MCP to near normal levels. In contrast, C3b/C4b receptor (CR1) tended to increase with granulocyte-CSF treatment in several cell lines. We simultaneously determined levels of decay-accelerating factor (DAF) and CR1 in these tumor cells, and tested susceptibility to C3 deposition via activation of the alternative C pathway. Of 21 cell lines we examined, 14 lacked CR1 and two lacked DAF; none, however, lacked MCP. A slight amount of C3 deposition was observed in some myeloid cell lines and EBV-infected B cell lines. However, C3 deposition did not reflect a defect in the regulatory proteins. Tumor cells bearing MCP, lacking CR1 or DAF, and undergoing no C3 deposition, may escape C attack due to the compensatory effect of MCP in the absence of the other regulatory proteins. High expression of MCP provides a convenient means for tumor cells to block C attack and survive in blood stream. We favor the interpretation that MCP is up-regulated in association with certain malignant disorders, and that cell differentiation results in a switch from an MCP-dominant state to a CR1-dominant state.

Antibodies, Monoclonal↗
PubMed1993

Complement activation in newborn infants with early onset infection.

The complement system is an important element in host defense. Quantitative deficiencies of total hemolytic complement activity and decreased C3 levels were reported in sera from normal neonates. However, little is known about complement activation products in the newborn. In a prospective study, complement activation products were determined in 32 healthy term neonates, in 41 neonates with colonization of their mothers, in 15 colonized neonates, and in 10 neonates with early onset infection. In all newborns, EDTA plasma was obtained within the first 6 h of life. The anaphylatoxin C3a-desArg was determined with a novel ELISA using an MAb reacting with a neoepitope of C3a-desArg. C3bBbP (alternative pathway convertase) and C1rsC1-inactivator (activation product of classical pathway) were measured with double-sandwich ELISA. C3 was determined by radial immunodiffusion. Plasma concentrations of C3a-desArg were similar in healthy term neonates and healthy adults, whereas diminished C3 levels were observed in the newborn infants. There were no significant differences between healthy neonates, neonates with colonized mothers, and colonized neonates. In neonates with infection, a significant elevation of C3a-desArg was found at the onset of the disease, resulting from alternative pathway activation. In contrast, the C1rsC1-inactivator complex showed no significant differences among healthy, colonized, and infected neonates. The anaphylatoxin C3a mediates inflammatory reactions such as vasodilatation and an increase in microvascular permeability and might therefore play an important role in severe neonatal infection.

Complement Activation↗