Dissociation of immune complexes and inactivation of bound antibodies by reducing agents.
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Antigen-Antibody Complex↗
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Venom of the ant Pseudomyrmex sp.: further characterization of two factors that affect human complement proteins.
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Animals↗
Adherence, augmented adherence, and aggregation of polymorphonuclear leukocytes.
Adherence of polymorphonuclear leukocytes to nylon fiber was found to be plasma-independent and distinct from the processes of augmented adherence, leukocyte aggregation, and inhibition of random leukocyte migration, all of which are dependent on "activated" plasma. Nylon fibers were unable to "activate" plasma, in contrast to the complement-activating agent zymosan. Prior incubation of plasma with antiserum to the third component of complement (C3) inhibited aggregation of polymorphonuclear leukocytes by plasma incubated with zymosan, and heat-inactivation blocked augmentation of adherence by treatment of plasma with zymosan.
Adult↗
The in vitro and in vivo effects of carrageenin on humoral and cellular factors of natural resistance.
The inhibitory effect of carrageenin, a sulfated algal polygalactose, on humoral factors of natural resistance is discussed. In dependence on dose and time, the influence of non-specific and specific bacteriolysis, on the in vitro and in vivo opsonic activity and on the course of infection was studied.
Animals↗
Defective regulation of chemotaxis in cirrhosis.
The presence of a severe leukotactic defect in cirrhotic patients has been confirmed. This defect is due to the presence of abnormally high levels of the chemotactic factor inactivator (CFI) in serums of patients with hepatic cirrhosis. This inactivator inhibits each of three different chemotactic factors tested and does so in an irreversible manner. As would be predicted by these results, generation of chemotactic activity in cirrhotic serums by a complement-activating agent is markedly impaired. Physicochemical features of CFI in cirrhotic serum differ slightly from that found in normal human serum. These results indicate the nature of the chemotactic defect in cirrhotic patients and may explain the increased susceptibility of these patients to bacterial infections and some of their reported defected in expression of cellular immunity.
Aminopeptidases↗
Levels of total haemolytic complement activity in paired dairy cow-newborn calf sera.
Total haemolytic complement (CH50) activities of sera obtained from newborn dairy calves and their corresponding dams were compared. The differences between the mean maternal and neonatal CH50 concentrations were significant (P less than or equal 0.001). The concentration of CH50 units/ml in sera from 16 calves was 52.0 +/- 21.4, whereas, for the cows it was 195.8 +/- 24.0. The ratio of cow: calf serum CH50 values averaged 4.24 with a range from 1.77 to 8.00. A positive rank correlation of 0.479 (P less than 0.05) was found between the CH50 titres in calves and their dams. Anticomplementary substances were not detected in calf sera. The possible relationships betweeen deficient CH50 levels in newborn calves and their susceptibility to infectious agents is discussed.
Age Factors↗
Hereditary angioedema controlled with danazol. Report of a case.
Hereditary angioedema is a condition which should be approached with caution and concern for the patient. The fact that the disease can be fatal cannot be overemphasized. The routine medical history should include questions aimed at identifying these patients. If the angioedema patient is to be treated, provisions must be made for maintenance of an adequate airway. This should include intubation if deemed necessary, and the practitioner should be prepared for a tracheostomy. Close observation following extubation is indicated. A case report in which the patient was controlled with danazol, a synthetic androgen, has been presented. The primary advantage of this drug is a decrease in the various side effects which have been associated with other therapeutic agents used previously in the treatment of hereditary angioedema.
Adult↗
Interaction of collagen with serum complement: inhibition of complement-mediated hemolysis.
Collagens from various vertebrate tissues were tested for their ability to consume complement (C) activity upon incubation in human serum or with isolated components of complement. 10 of 12 collagens tested had anticomplementary activity. The heat-denatured form of collagen, gelatin, was found weakly anticomplementary, but elastin was found inactive in the interaction with C. Inactivation of C is a reaction which is dependent on the time of incubation and the collagen concentration and partially dependent on the temperature of incubation. Most collagens depleted C from human serum in presence of cation chelators, EDTA and EGTA, whereas the large part of anticomplementary activity of soluble collagens obtained from rat skin was abolished in presence of EDTA. Evidence is presented that two different principles in collagens play a role in inactivation of C. A factor, contained in insoluble collagens and inhibitable by mild oxidation with periodate, inactivates C1 directly even in presence of chelating agents. Another principle, contained in soluble and insoluble collagen and resistant to periodate treatment, depletes C in serum by utilization of C via the alternate pathway (the C3 shunt).
Animals↗
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↗
The relation of rheumatoid arthritis to hypogammaglobulinemia.
The following hypothesis is proposed. Hypogammaglobulinemia is produced by an excess of normal 7S complement-fixing anti-immunoglobulin which is specific for "altered" Fc portions of immunoglobulin. This is present lesser amount in normal blood, is not reactive with the native immunoglobulins of blood, and plays a part in controlling the normal level of antibody production. When it is present in excess, some patients respond by producing also an excess of normal non-complement-fixing 7S anti-immunoglobulin of the same specificity as well as classical 19S IgM rheumatoid factor. These latter agents successfully prevent the hypogammaglobulinemia but they produce "side effects". These "side effects" constitute classical rheumatoid arthritis.
Agammaglobulinemia↗
Trypanosoma (Schizotrypanum) dionisii: effect of various agents on attachment and entry to macrophages in vitro and on morphogenesis.
The attachment and entry of Trypanosoma dionisii to mouse peritoneal macrophages in vitro were studied. Both occurred to a similar extent whether parasites were alive or heat-killed, and whether macrophages were obtained from normal or immunized mice. Attachment occurred equally at 4 and 37 degrees C, but entry only occurred at the higher temperature. Neither was affected by pretreatment of parasites with active or inactivated complement. Entry, but not attachment, was inhibited by cytochalasin B; both were inhibited by trypsin. Immune mouse plasma (if inactivated) stimulated attachment but not entry (within 24 h). It also stimulated intracellular replication of T. dionisii by multiple fission and subsequent differentiation (probably within macrophages) to small extracellular trypomastigotes. No extracellular parasite and only scanty intracellular forms survived 120 h in cultures containing non-inactivated immune mouse plasma. It was concluded that attachment (in the absence of antibody) occurred to non-specific receptors in the macrophage membrane and was followed by phagocytosis of the parasites rather than their active penetration of the cell.
Animals↗
Circular dichroism of C3a anaphylatoxin. Effects of pH, heat, guanidinium chloride, and mercaptoethanol on conformation and function.
Circular dichroism spectra for C3a anaphylatoxins (protein fragments generated enzymatically in serum during activation of the third component of complement (C3)) from human and porcine sources were compared in the region of 190 to 250 nm. The spectra were indistinguishable in this region, although an estimated difference of approximately 20% exists between the primary structures of human and porcine C3a. Calculations indicated a total of 40 to 45% alpha helical content based on either the 208 or 222 nm extremum of the CD spectra. Addition of either mercaptoethanol or 6 M guanidinium chloride to human C3a produced a marked decrease in the mean residue ellipticity centered at 222 nm without irreversibly affecting the biological activity. Simultaneous addition of mercaptoethanol and guanidinium chloride virtually eliminated the CD contribution at 222 nm and resulted in more than 90% inactivation of the anaphylatoxin. Removal of the denaturant and reducing agent restored both the biological activity and the CD spectrum of C3a. Heat treatment or reduction and alkylation of human C3a produced biologically inactive and conformationally modified anaphylatoxin. In contrast, C3a inactivated by enzymatic removal of the COOH-terminal arginyl residue was structurally unchanged as judged by CD measurements. Consequently, it is proposed that in addition to the essential COOH-terminal arginyl residue, a highly ordered conformation is required for biological functionality of the C3a molecule.
Animals↗
Quantitative studies on cell-mediated immunity in the pleural cavity of guinea-pigs.
Intrapleural injection of PPD into CFA-sensitised guinea-pigs produced a reaction having many of the characteristics of classical delayed hypersensitivity. Quantitative investigations of the time course of this reaction showed that it was typified by an initial delay in the onset of increased vascular permeability, which reached its peak between 12 and 18 hr. The cellular response in the pleural cavity followed a similar pattern, attaining maximum levels between 18 and 24 hr. Mononuclear cells dominated the reaction from 12 to 48 hr. The histological appearance of the lung tissue was also studied. Treatment with Cobra venom factor, a complement-depleting agent, failed to modify this reaction. Cyclic AMP levels were assayed for both the cellular and cell-free exudates.
Animals↗
Severe staphylococcal disease associated with allergic manifestations, hyperimmunoglobulinemia E, and defective neutrophil chemotaxis.
Neutrophil granulocyte function was determined in three patients with systemic staphylococcal infection, clinical manifestations of generalized allergic disease, and hyperimmunoglobulinemia E. Each of the patients had urticarial skin rashes before or at the time of development of staphylococcal suppurative lymphadenitis, pneumonia, or sepsis. Neutrophil chemotaxis, random migration, phagocytosis, and bactericidal capacity were assessed to determine if an abnormality in these functions might have contributed to the development of severe staphylococcal infections. Each of the three patients with generalized urticaria was found to have a marked defect in neutrophil chemotaxis. The mean chemotactic index of the patients was 12 +/- 4, whereas that of 20 controls was 72 +/- 11. Neutrophil random migration, phagocytosis, and bactericidal capacity were normal in each patient. The serum or plasma of the patients did not inhibit chemotaxis of control neutrophils and did not contain an increased concentration of the chemotactic-factor inactivator found in normal serum. Treatment of the neutrophils of these three patients with the competitive histamine H2 receptor blocking agent, burimamide, produced a significant increase in chemotactic responsiveness. These studies suggest the possibility of pharmacologic modification of neutrophil granulocyte function.
Burimamide↗
Murray Valley encephalitis in Australia, 1974: antibody response in cases and community.
Fifty-three patients accepted on clinical grounds as cases of Murray Valley encephalitis (MVE) in Australia in 1974 were examined for antibody to MVE virus. Only one (who died early in the disease and whose diagnosis was confirmed by virus isolation) did not develop antibody; 13 patients showed stationary or single convalescent titres not diagnostic of recent infection, but other evidence that infection was recent was obtained in eight; 39 showed significant rise or fall in titre confirming recent infection. Haemagglutination-inhibition (HI) was more effective in establishing a diagnosis than complement-fixation (CF) although both tests were of value. Patients varied widely in timing and magnitude of rise and fall of titre. Two showed late rises in antibody titre which raises the possibility of recrudescent persisting infection. CF titres were enhanced in some sera by increase in the number of units of antigen used and by inactivation at 56 degrees C rather than 60 degrees C. Five patients with clinically-acceptable diagnoses of MVE (and one with minor illness) showed higher HI titres to Kunjin than to MVE virus. The results in several cases suggest that Kunjin virus was the infecting agent. In others it is possible that MVE infection had occurred in patients with pre-existing Kunjin antibody. HI reactivity to MVE virus was found in IgM fractions of sera taken for at least 40 days and in some cases for over 100 days after onset of symptoms. IgM fractions gave similar titres to MVE and Alfuy virus but clearly distinguished MVE-Alfuy and Kunjin viruses. HI antibody to MVE virus was found in about 10% of sera from family contacts or neighbours of patients with encephalitis, and in a similar proportion of patients in Victoria with various febrile illnesses not accepted as MVE. One patient with minor illness had antibody response to Kunjin virus. 2589 sera from pathology laboratories in towns in the Murray Valley gave additional evidence of community immunity to flaviviruses and suggested some increase in the proportion reactive between January and May 1974. HI and plaque reduction tests on these sera also gave evidence of antibody to Kunjin virus in the Murray Valley.
Adolescent↗
The induction of augmented granulocyte adherence by inflammation. Mediation by a plasma factor.
The adherence of granylocytes to surfaces, measured in vitro in nylon fiber columns, is inhibited by in vivo administration of anti-inflammatory agents. Therefore, the effect of inflammation itself was assessed in blood from patients with acute inflammatory diseases. Mean adherence in these patients was twice normal (56.4 +/- 5.6% vs. 29.4 +/- 5.2%); their plasma contained a factor that augmented adherence of normal cells to 47.5 +/- 5.6% whereas the patient's cells showed a normal level of adherence (34.0 +/- 6.8%) when resuspended in normal plasma. Although exudate fluid from exprimental inflammation also contained the augmenting factor, cells from the exudate maintained their high level of adherence after washing and suspension in normal plasma. The augmenting factor detected in plasma from patients with inflammation was not present in serum and was inactivated by heating plasma to 56 degrees C for 30 min; restoration of augmenting activity was accomplished by addition of 20% guinea pig serum to the heat-treated plasma. Because the guinea pig serum itself did not increase adherence when added to normal plasma, it appears that the augmenting factor is heat-stable, but requires a heat-labile cofactor like complement. Sephadex G-200 fractionation of inflammatory plasma showed adherence-augmenting activity in the majority of fractions, with peak activity in the fractions corresponding to approximate molecular wts of 30,000, 160,000 and 400,000.
Adrenal Cortex Hormones↗
Reconstruction of cells by Sendai virus-induced fusion of cell fragments.
Large numbers of animal cells can be enucleated by centrifugation in the presence of cytochalasin. The nuclei (minicells) obtained by this technique are surrounded by a thin rim of cytoplasm and a cell membrane. The cytoplasms (anucleate cells) contain cytoplasmic organelles and are capable of protein synthesis. By themselves, these cell fragments are not viable under usual culture conditions for longer than 2 days after enucleation. They can, however, be fused by UV-inactivated Sendai virus to form reconstituted cells. Nuclei from rat myoblasts have been combined with cytoplasms from mouse fibroblasts. The resulting reconstituted cells are viable and multiply rapidly in vitro. Enucleation or disruption of "micronucleated" cells, cells in which the genome has been fragmented into many small micronuclei by prolonged exposure to antimitotic agents results in microcells. These cell fragments are subdiploid and may contain as little as a single chromosome. Fusion of microcells from normal cells with intact mutant cells offers a method of transferring complementing chromosomes into genetically defective cells. Specific areas in which reconstitution techniques should prove useful include studies of gene expression, cell differentiation, and the dependence of mitochondria on nuclear genes. Microcell hybrids could be useful in chromosome mapping and gene complementation analysis.
Animals↗
C1q (c1) receptor on human platelets: inhibition of collagen-induced platelet aggregation by C1q (C1) molecules.
Hemolytically active human C1q incubated with EA before the addition of complement inhibited the immune hemolysis. On the contrary, heat-inactivated preparation (30 min 56 degrees C) was ineffective. Preincubation of EA with bovine collagen also resulted in a decreased hemolysis. When aggregation was measured by a turbidimetric method in citrated human platelet-rich plasma, it was found that hemolytically active human C1q (C1) alone does not induce platelet aggregation. However, in its presence the platelets failed to aggregate or exhibited a significantly reduced aggregation response to bovine collagen. The inhibition by C1q depended on the preincubation time with platelets. Heat treatment (30 min 56 degrees C) destroyed the inhibitory action of C1q (C1). The effect of C1q proved to be highly specific because different C1q preparations at their inhibitory doses in collagen-induced platelet aggregation did not influence the response to other aggregating agents (bovine thrombin, ADP, horse anti-human thymocyte globulin, goat anti-baboon platelet antiserum). The results prove that collagen and C1q are capable of binding to the same site(s); namely, to those of EA and human platelets; furthermore, they suggest the presence of a receptor for C1q (C1) on human platelets.
Adenosine Diphosphate↗