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Biomedical subjects

A C Allison

Publications and source records attributed to A C Allison.

At least 127 records · Page 7Linked to original sources
PubMed1985

Acne-like chronic inflammatory activity of Propionibacterium acnes preparations in an animal model: correlation with ability to stimulate the reticuloendothelial system.

The ability of strains and fractions of killed propionibacteria suspensions to produce chronic rat ear inflammation after intradermal injection of 70-micrograms aliquots was highly correlated with production of splenomegaly in the mouse after i.p. injection of 1.4 mg Propionibacterium acnes strains CN 6134, VPI 0009, ATCC 11828, and UCLA SC and N1 produced a 2- to 3-fold increase in rat ear thickness and a 5- to 7-fold increase in mouse spleen weight 15 days post injection. In contrast P. granulosum CN 5888, P. acnes UCLA 6S and periodated, acetylated, or 12-h cultures of VPI 0009 were inactive or weakly active as stimulators of chronic ear inflammation and splenomegaly. Active strains produced in the rat ear a transepidermal elimination response characterized by follicular encapsulation and the formation of secondary comedones. These effects correlated with persistence of phagocytized bacteria within macrophages. Furthermore, when rats were first immunized and then challenged with active strains of P. acnes, an increased sensitivity to low doses of P. acnes and a chronic exacerbation of inflammation was observed.

Acne Vulgaris↗
PubMed1985

A monoclonal antibody against basal cells of human epidermis. Potential use in the diagnosis of cervical neoplasia.

A murine monoclonal antibody was generated against human skin cells obtained from psoriatic plaques. The antibody, called VM-2, recognizes an epitope expressed on the basal cell layer of human skin and other epithelia. VM-2 also binds to cultured cells from a variety of human carcinomas including HeLa cervical carcinoma, A-431 vulvar carcinoma, A-549 lung alveolar carcinoma, and SCL-1 skin squamous cell carcinoma cells. In several primary human cell lines, including fibroblasts, endothelial cells, and cells from the hematopoietic lineage, the antigenic site recognized by VM-2 could not be detected. The cellular antigen when immunoprecipitated by VM-2 from both normal and transformed cells appears to be proteins of approximately 100,000 and 120,000 mol weight. In frozen sections from human tumor-containing tissues, VM-2 labels skin, cervical, and lung squamous carcinoma cells, as well as skin basal carcinoma cells. Malignant cells present in exfoliative smears from epidermoid invasive neoplasias of the cervix are also selectively recognized by VM-2 in distinction to normal squamous cervical cells. VM-2 is thus directed against an antigen associated with neoplastic cells when applied in selected sites of exfoliative cytology. This monoclonal antibody represents a new reagent that should prove useful in the diagnosis of cervical neoplasia.

Antibodies, Monoclonal↗
PubMed1984

Lipopolysaccharide hyperreactivity of animals infected with Trypanosoma lewisi or Trypanosoma musculi.

Rats and mice infected with Trypanosoma lewisi and Trypanosoma musculi, respectively, showed hyperreactivity to lipopolysaccharide (LPS) from gram-negative bacteria. Fatal shock could be precipitated with a dose of LPS 100 to 1,000 times less in infected compared with noninfected animals. In trypanosome-infected rats and mice, extensive liver damage was evident after LPS challenge. These animals showed a pronounced hypoglycemia, marked elevation of blood aspartate transaminase level, and diffuse severe degeneration and total depletion of glycogen in hepatocytes. Only minor changes were observed in noninfected animals given the same dose of LPS. No mononuclear phagocytic cell infiltration was observed in the liver of infected animals. The most striking change was the great increase in size and the probable increase in phagocytic activity and number of sinusoidal Kupffer cells. We suggest that elevated Kupffer cell activity in trypanosome-infected animals may play a role in LPS-induced hepatotoxicity.

Animals↗
PubMed1983

Polyamine oxidase mediates intra-erythrocytic death of Plasmodium falciparum.

Using a number of established culture strains of Plasmodium falciparum, the effects of the addition of polyamine oxidase and spermine on the intra-erythrocytic forms were studied. Cultures to which polyamine oxidase and polyamines were added contained only degenerate parasites but if one or other were added alone the cultures were similar to the controls. The effects were confirmed by 35S-methionine incorporation.

Animals↗
PubMed1983

Experimental erythrocyte autoimmunity prevented by suppressor T cells in mice treated with Cyclosporin-A.

Mice injected with rat erythrocytes produce erythrocyte autoantibodies and suppressor cells that inhibit autoantibody production without inhibiting the net production of antibodies against rat RBC. Here it is shown that injecting mice with Cyclosporin-A daily for up to 13 days during the course of injections of rat RBC significantly inhibits autoantibody production. Antibody production against rat RBC was also inhibited. The Cyclosporin-A-treated mice that did not produce autoantibodies produced suppressor cells that inhibited autoantibody production in adoptive transfer experiments. These suppressor cells, which did not inhibit antibody production against rat RBC, were destroyed by treatment with anti-Thy 1.2 serum and complement. From the results, it is suggested that in this experimentally induced autoimmune disease, suppressor T cells may be activated and/or preferentially spared in Cyclosporin-A-treated mice.

Anemia, Hemolytic, Autoimmune↗
PubMed1983

Alternative pathway activation of complement by African trypanosomes lacking a glycoprotein coat.

An in vitro culture Trypanosoma congolense cell line was established using the mammalian cell feeder layer system. One of the principle characteristics of this parasite was its ability to multiply in culture at 35 degrees C, as an uncoated trypanosome (lacking a glycoprotein surface coat) unlike the original blood stream form from which it was derived. This trypanosome was lysed when incubated in normal human serum in contrast to the parasite which possessed a surface coat. The lytic reaction as inhibited by EDTA but not EGTA and occurred in C2-deficient serum, demonstrating the involvement of the alternative pathway of complement activation. Similar results were obtained with procyclic forms of T. congolense and T. brucei brucei which also lacked surface coats. The results suggest that the glycoprotein surface coat protects the parasite by masking sites on the plasma membrane which are capable of promoting alternative pathway activation.

Animals↗
PubMed1983

Natural agglutinins to African trypanosomes.

Agglutinins to uncoated culture forms of the African trypanosomes, T. congolense and T.b. brucei were detected in sera from a variety of mammals not exposed to the parasites. The agglutinins in bovine serum were shown to be specific antibodies with opsonic properties selective for the species of trypanosome. These findings suggest a possible role for the glycoprotein coat in preventing access of cross-reacting antibodies to the plasma membrane of African trypanosomes.

Adult↗
PubMed1983

Serum containing tumor necrosis factor is cytotoxic for the human malaria parasite Plasmodium falciparum.

Sera (BCG-lipopolysaccharide [LPS] serum) were obtained from mice infected with Mycobacterium bovis BCG 2 h after intravenous administration of bacterial endotoxin (LPS). Varying concentrations of sera were added to cultures of Plasmodium falciparum-infected human erythrocytes; parasite viability was assessed by hypoxanthine incorporation after 4 days in culture. At concentrations of 1 to 3%, cultures treated with BCG-LPS serum showed a two- to threefold increase in hypoxanthine incorporation; at higher concentrations (4 to 8%), hypoxanthine incorporation fell to 2 to 5% of that in control cultures. Concurrent assays with control sera (from untreated mice or mice treated with BCG or LPS alone) caused some stimulation but no inhibition at up to 8% concentration. Examination of cultures treated with BCG-LPS serum showed morphological, deterioration of parasites within erythrocytes. The presence of tumor necrosis factor in the BCG-LPS serum was confirmed by using a standard L-cell cytotoxicity assay. In addition, rabbit antiserum against partially purified tumor necrosis factor protected intraerythrocytic forms of P. falciparum from the toxic effects of BCG-LPS serum. These data suggest that the factor in BCG-LPS serum that is toxic to P. falciparum in human erythrocytes is antigenically similar or identical to tumor necrosis factor. This nonantibody mediator of killing may play a role in human malaria.

Animals↗
PubMed1983

The role of cell-mediated immune responses in resistance to malaria, with special reference to oxidant stress.

Asexual blood forms of malaria parasites are microaerophilic and sensitive to oxidant stress. Plasmodium falciparum and some other species of malaria parasites undergo schizogony attached to endothelial cells of postcapillary venules, where oxygen tensions are low. Acquired immune responses to all forms of malaria parasites so far investigated are thymus dependent. Animals deprived of T lymphocytes do not recover from the infections and cannot be immunized against malaria parasites. In contrast, animals unable to make antibodies recover normally from some primary infections, e.g. with Plasmodium chabaudi, and when rescued by chemotherapy from other species of malaria parasite develop lasting, nonsterile immunity. Immunity to malaria can be transferred in mice by T lymphocytes of the Ly1+ phenotype, but transfer of B lymphocytes together with this T-cell subset increases the effectiveness of immunity to Plasmodium yoelii. Thus, antibodies facilitate recovery from some primary malaria infections and increase the effectiveness of cell-mediated immune responses in these infections. Mice of the A strain are highly susceptible to malaria and are unable to increase the number of mononuclear cells in the spleen during the course of the infections. It is postulated that T lymphocytes responding to parasite antigens release factors that stimulate the proliferation of effector cell precursors and their recruitment into the red pulp of the spleen. In this site, the liver and probably the peripheral circulation, effector cells bind to the surface of parasitized erythrocytes and are activated to release superoxide (O2-). The consequent exposure to oxidant stress can lead to degeneration of parasites in erythrocytes. This effect on the parasites can be prevented by agents chelating metals, which suggests that iron-catalyzed lipid peroxidation and consequent K+ loss, or inactivation of metal-containing enzymes, may be the mechanism by which oxidant stress kills the intracellular parasites. Antibodies on the surface of schizont-infected cells could facilitate binding of effector cells and trigger O2- release, thereby acting synergistically with cell-mediated immunity. Inherited traits, such as abnormal hemoglobins and G-6-PD deficiency, and acquired cell-mediated immunity both subject malaria parasites to oxidant stress and may reinforce one another, increasing the chances of survival of children bearing these traits during the dangerous years of first exposure to malaria in areas where the disease is endemic.

Animals↗
PubMed1983

Antitrypanosomal activity of sinefungin.

Sinefungin, a naturally occurring antifungal antibiotic nucleoside containing an ornithine residue, linked by a C-C bond to C-5' of adenosine, cures mice infected with Trypanosoma brucei brucei, T. congolense, or T. vivax; the effect of the drug is more pronounced towards T. congolense. Anti-trypanosomal activity of sinefungin could be the result of the inhibition of transmethylation reactions or of polyamine biosynthesis--or both--in parasites.

Adenosine↗
PubMed1982

A radical interpretation of immunity to malaria parasites.

Asexual forms of malaria parasites in erythrocytes are sensitive to oxidant stress. Immunity to these parasites is thymus-dependent and may be mediated by the blinding of effector cells (macrophages or natural killer cells) to the surface of parasitised cells, with concomitant production of the superoxide anion (O2-). This can lead to degeneration of parasites in erythrocytes. Antibodies can facilitate the binding of effector cells to parasitised erythrocytes, reinforcing the effects of cell-mediated immunity. Plasmodium falciparum is more sensitive to oxidant stress in human erythrocytes with abnormal haemoglobins and glucose-6-phosphate-dehydrogenase deficiency than in normal erythrocytes. Thus cell-mediated immune responses, by producing oxidant stress, could act synergistically with these inherited traits to increase the chances of survival of children during the dangerous years of first exposure to malaria.

Antibody Formation↗
PubMed1982

Polyamine oxidase-mediated killing of African trypanosomes.

African trypanosomes, Trypanosoma brucei brucei, T. vivax and T. congolense, were killed when incubated in vitro with ruminant sera in the presence of exogeneous spermidine, and were non-infective for mice. Purified polyamine oxidase in the presence of spermidine-mediated similar killing of trypanosomes. The abundance of polyamine oxidase activity in ruminant sera which can react with polyamines to produce products with cytotoxic properties may explain the trypanosome killing. This system may contribute to non-specific parasite killing in vivo.

Animals↗
PubMed1981

Theileriosis: cell-mediated and humoral immunity.

The protozoan parasite of cattle Theileria parva transforms lymphoid cells into permanently proliferating cell lines. Antibodies reacting with parasite antigens can be detected by several methods, but there is no evidence that they are protective. Two cellular responses to infection have been found. In immune animals powerful cytotoxicity restricted to syngeneic infected cells rapidly appears; this is thought to be mediated by T-lymphocytes and to play a major role in resistance to reinfection. In primary infections cytotoxicity against allogeneic infected and xenogeneic cells is observed late. This is thought to be due to activation of a nonspecific cytotoxic system, which contributes to the lymphocytolysis and panleukopenia, a prominent feature of the disease. If mounted early enough, the nonspecific effector mechanism could also contribute to recovery from a primary infection, when it occurs.

Animals↗
PubMed1980

Cytolysis of fibroblasts by C3a.

C3a was found to be more cytolytic to transformed than to primary fibroblast cultures from mouse and man. Fibroblasts made quiescent with caffeine were lysed by the same concentrations of C3a as untreated cells. These findings may have implications in tumour immunity.

Animals↗
PubMed1980

Differences in susceptibility of various mouse strains to haemoprotozoan infections: possible correlation with natural killer activity.

Striking differences in the susceptibility to P. chabaudi and B. microti infections among different strains of mice are described. In most of the strains, both parasites induce a moderate, transient parasitaemia, followed by recovery. However, in the A strain P. chabaudi is rapidly lethal and B. microti induces a parasitaemia which persists for life in most animals. In contrast B10.A mice, which have the same H-2q haplotype as the A strain, recover from both infections. In first crosses (A X B10.A)F1 mice are uniformly resistant. Among other correlates, NK cells activity may be relevant. This activity is known to be high in strain of mice which are resistant to both of the parasites studied, such as C57B1 and CBA mice, and low in the susceptible A strain. We have examined the spleen weight, total cell number and NK activity at different times after infection. In the resistant strains there is a rapid increase in size and cell number which is still more marked during recovery. NK activity increases greatly during the infection; this is especially remarkable considering the dilution of nucleated cells with erythrocytes precursors. In contrast, in A mice cell numbers of NK activity remain almost unchanged. Thus, marked activation of NK cells occur, in resistant strains but not in susceptible ones. Possible mechanisms of activation of these cells and their effect in haemoprotozoan infections are discussed.

Animals↗