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Biomedical subjects

A C Allison

Publications and source records attributed to A C Allison.

At least 163 records · Page 9Linked to original sources
PubMed1979

Protection of pregnant mice with phospholipase C and with Arvin against foetal death induced by bacterial lipopolysaccharide.

Injection of bacterial lipopolysaccharide into pregnant mice resulted in fibrinogen accumulation, thrombosis and haemorrhage in the placental tissue and foetal death. Depletion of circulating fibrinogen by a thrombin-like enzyme from the venom of Malayan pit viper, Arvin, prevents foetal death. Foetal protection was also obtained by treating the mothers with a preparation of phospholipase C from Bacillus cereus known to inactivate tissue thromboplastin. It is suggested the lipopolysaccharide causes foetal death by inducing thrombosis as a consequence of activation of placental thromboplastin.

Ancrod↗
PubMed1979

The use of indium-111 for studies of cytotoxicity mediated by lymphocytes or by antibodies and complement.

Mouse P815 mastocytoma cells, Meth A sarcoma cells and human MRC5 fibroblasts and peripheral blood mononuclear cells were labelled with 111In, 51Cr or 125IUdR and their release from the cells measured. Spontaneous release of 111In from the cells in cultures was less than half that of 51Cr and was comparable to the release of 125I. When 111In-labelled P815 cells were lysed with antibodies and complement or with sensitized lymphocytes the label was released rapidly. 111In is a convenient label in short- as well as in long-term in vitro cytotoxicity studies because of its high labelling and detecting efficiency and its stable cell association.

Animals↗
PubMed1978

Role of mononuclear infiltrating cells in pathogenesis of hepatitis.

Mice that have been injected with Corynebacterium parvum have mononuclear-cell infiltrates in the liver lobules. In such mice a small dose of lipopolysaccharide endotoxin produced a lethal hepatitis, with high serum-transaminase concentrations, glycogen depletion, and hypoglycaemia. It is suggested that lipopolysaccharide triggers the release from the infiltrating mononuclear cells of factors toxic for hepatocytes. Similarly certain parasitic and virus infections and graft-versus-host reactions can sensitise mice to the induction of hepatitis by exposure to small doses of lipopolysaccharide. This model may be applicable to human hepatitis.

Animals↗
PubMed1978

Absence of a newly described cytochrome b from neutrophils of patients with chronic granulomatous disease.

A unique cytochrome b which becomes incorporated into phagocytic vacuoles has been described in human neutrophils. This cytochrome b appears to be situated in the plasma membrane of these cells, and acts as a component of the microbicidal oxidase system. Absence or gross abnormality of this cytochrome b was demonstrated in all four patients with chronic granulomatous disease who were investigated, and reduced concentrations in two mothers known to be carriers of the disease.

Child↗
PubMed1978

Tissue thromboplastin activity of isolated human monocytes.

Certain agents that induce spreading of or increased content or release of lysosomal enzymes from human monocytes also induce a dramatic increase in tissue thromboplastin content of the cells. The increase is inhibited by cycloheximide and actinomycin D and does not appear in granulocyte, lymphocyte or platelet populations treated in the same way. The effect of several other substances on the development of monocyte tissue thromboplastin activity is reported.

Blood Coagulation↗
PubMed1978

Extensive prolongation of rabbit kidney allograft survival after short-term cyclosporin-A treatment.

The fungal metabolite cyclosporin A has been administered daily at 25 mg/kg to nephrectomised rabbit recipients of a single renal allograft. After only 4 weeks of daily administration, rejection was prevented for long periods without the need for other immunosuppressive therapy. Renal function has been excellent in all cases, rejection episodes have not been encountered except in a small percentage of animals, and the surviving recipients are still in excellent health 3-6 months after transplantation. The possiblity that clones of responding lymphocytes might be selectively killed by this agent was suggested from earlier experiments and prompted this study. If toxicity is not encountered in man cyclosporin A may prove valuable in preventing rejection of organ and bone-marrow allografts and might be useful in treating some leukaemias of lymphoid origin.

Administration, Oral↗
PubMed1978

The role of macrophage activation in chronic inflammation.

The macrophage is the characteristic cell type in chronic inflammatory reactions, in the rheumatoid synovium, as in other sites. When macrophages are activated, considerable synthesis of enzymes and other proteins occurs. Macrophages can be activated by (i) products of activated lymphocytes, (ii) immune complexes and (iii) the complement cleavage product C3b. Among the many consequences of macrophage activation are (i) secretion of hydrolytic enzymes, (ii) cleavage of C3 into C3a, which is cytolytic, and C3b, (iii) production of tissue thromboplastin, a powerful procoagulant, and (iv) formation of polyamine oxidase, which in the presence of appropriate substrates generates factors that lyse or limit the proliferation of tumour cells, lymphocytes and micro-organisms. The relevance of these observations to the pathogenesis of chronic inflammatory reactions is discussed.

Animals↗
PubMed1978

Specific lethality of silica for human peripheral blood mononuclear phagocytes, in vitro.

Human peripheral blood mononuclear cells, cultured in the presence of 100 microgram/ml protein-coated silica particles, were studied to determine changes in number and function of monocytes, immunoglobulin bearing (B), sheep red blood cell rosetting (T) lymphocytes and the effector cells of antibody dependent cell-mediated cytotoxicity (ADCC). After 24-48 h, phagocytic cells were effectively eliminated from culture but there was no significant reduction in number or function of T or B lymphocytes or in ADCC to cell line targets. ADCC to erythrocyte targets was inhibited but not completely blocked. It is concluded that silica is a specific toxin for human peripheral blood mononuclear phagocytes and may be useful in in vitro immunological studies as a means of eliminating or determining the role of these cells without resort to separation methods which result in losses of cells other than monocytes.

Animals↗
PubMed1978

Tracing the fate of oxygen consumed during phagocytosis by human neutrophils with 15O2.

1. The metabolism of oxygen by phagocytosing neutrophils was traced by using 15O2. 2. The isotope did not exchange with the incubation medium or cells to an appreciable extent and unmetabolized oxygen was readily eluted by gassing the cell suspension. 3. The polarographic measurements of oxygen consumption closely paralleled the recovery of metabolized 15O2. 4. Almost all the metabolized 15O2 was converted into water, both in the presence and absence of KCN, supporting the concept that the oxygen consumed by neutrophils is converted into H2O2. It is unlikely that an appreciable proportion of this oxygen is incorporated into the organic composition of the cell or of the ingested micro-organism.

Humans↗
PubMed1978

Effects of cytochalasin B on endocytosis and exocytosis.

The complex effects of cytochalasin B on endocytosis and exocytosis are reviewed. Cytochalasin B inhibits phagocytosis by both mononulcear phagocytes and polymorphonuclear leukocytes but it does not affect the micropinocytic activity of mononulear phagocytes and other cell types. Cytochalasin B causes increased selective release of acid hydrolase from phagocytic cells but its effect on other secretory cells is more variable, stimulating secretion by some cell types, inhibiting secretion in others and having no effect at all in some instances. The possible mechanisms of action of cytochalsin B are discussed with particular emphasis being placed on its effect on the activity of various protein components of cellular contractile systems. We suggest that many of the biolgoical effects of cytochalasin B may be accounted for by such effects.

Animals↗
PubMed1978

Macrophage secretion and the complement cleavage product C3a in the pathogenesis of infections by mycoplasmas and L-forms of bacteria and in immunity to these organisms.

Mouse peritoneal macrophages in culture exposed to Mycoplasma pulmonis show marked biochemical changes. This micro-organism induces the release of hydrolytic enzymes from macrophages. The release is time- and dose-dependent and is not associated with loss of the cytoplasmic enzyme lactate dehydrogenase or any other sign of cell death. Secretory products of macrophages may play a role in the pathogenesis of chronic inflammatory responses elicited by mycoplasma infections. One of the products of activated macrophages is the complement cleavage product C3a. Purified C3a was incubated with M. hominis, M. pulmonis, Proteus mirabilis and an L-phase variant of this organism. All mycoplasmas and the L-phase variant were lysed by low concentrations of C3a, whereas the bacterial form of Pr. mirabilis was resistant.

Animals↗
PubMed1978

Production of the complement cleavage product, C3a, by activated macrophages and its tumorolytic effects.

Mouse peritoneal macrophages were activated in serum-free culture with lipopolysaccharide, dextran sulphate or C3b. They were found to liberate into the culture medium a cytolytic factor and a factor which was pharmacologically indistinguishable from C3a. The cytolytic activity was neutralized by antiserum against C3a. These results suggest that macrophages can be activated by C3b (or agents that generate C3b) to cleave C3, which they themselves produce. In this way the activated macrophages form C3a, which appears to be a major factor in macrophage-mediated cytolysis. These findings have implications in tumour immunity and in the pathogenesis of inflammatory reactions.

Animals↗
PubMed1978

Protection of mice against haemoprotozoan Babesia microti with Brucella abortus strain 19.

When Brucella abortus strain 19 is given intraperitoneally to mice it protects them against subsequent infection with large doses of Babesia microti. The protection obtained was more effective when B. abortus was given intraperitoneally than when it was injected subcutaneously. This non-specific protection seems to be best explained by the stimulation of macrophages so as to release a mediator which limits the intracellular replication of the parasites.

Animals↗