Resistance of mice to Naegleria meningoencephalitis transferred by immune serum.
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Biomedical subjects
Publications and source records attributed to A Ferrante.
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The present study emphasises the importance of the mononuclear phagocytic system of the rat in immunity to infections with Trypanosoma lewisi. Despite the great increase in the weight of the spleen, the liver played a major role in removing the parasites from the circulation. No evidence could be obtained that removal of the parasites was related to the lytic activity of specific antibody and complement.
Data presented show that during the course of a Trypanosoma lewisi infection in rats there was both an activation of the phagocytic cells of the liver and spleen and an increase in their numbers. There was a marked lymphoid hyperplasia in the white pulp of the spleen with an increase in the number and size of the lymphoid follicles. Degenerative changes occurred in the liver parenchymal cells during the infection, and at certain stages large numgers of mononuclear cells were observed in the vascular sinusoids and other vessels of the liver.
This paper describes a simple quantitative assay for albastin, a factor present in the serum from rats infected with Trypanosoma lewisi, which prevents the division of the parasite. The assay measures in vitro the inhibition of the incorporation of 3H-TdR into the DNA of T. lewisi in the presence of serum from infected animals. Utilising this method, one can measure the titre of albastin in a particular serum sample and the time and duration of its appearance in the circulation of infected rats.
Activation of the alternative pathway of complement by Candida albicans was examined using a chemotactic assay. Two serologically defined strains and eight clinical isolates of Candida albicans were used in these experiments. The results showed that all ten strains of Candida albicans were capable of alternative complement pathway activation. These findings may provide an insight into host resistance to this infection.
Two of 5 children in one family presented with unique facies, proportionate small stature and sensorineural deafness-mutism. One of the children who had a history of recurrent infections, was shown to have a defect of leukocyte chemotaxis. Although impairment of chemotaxis could not be demonstrated in the other affected sibling, it is unlikely that the association of a previously undescribed syndrome and a rare disorder of chemotaxis is a chance occurrence.
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Naegleria fowleri, a free-living ameboflagellate, is the causative organism of primary amebic meningoencephalitis. Intranasal inoculation of N. fowleri in mice produces an infection similar to human disease. Mice immunized with live N. fowleri by intraperitoneal injection were found to be more resistant to subsequent intranasal challenge. These results may provide a lead to the development of immunotherapy for this virulent disease for which satisfactory chemotherapy is presently unavailable.
In vitro mitogen-induced proliferative responses of human lymphocytes were inhibited by concentrations of quinine normally attainable during therapy of malaria infections. The clinical implications of these findings are discussed.
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The results presented below show that the dividing and adult forms of T. lewisi share common antigens and indicate that the persistence of adult forms in the circulation of rats immune to reinfection is not due to a change in surface antigens as has been postulated. Using a rabbit anti-rat immunoglobulin serum, the presence of rat immunoglobulins on the surface of adult trypanosomes could be demonstrated. These immunoglobulins were not complement-fixing or opsonic. It is suggested that these immunoglobulins are responsible for the persistence of the adult forms in the circulation of the rat.
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The origin of illness and pathology in malaria is now largely attributed to high levels of circulating tumour necrosis factor (TNF), released from cells of macrophage lineage after triggering by the products of malarial schizogony. The role of lymphocytes and their products in malarial pathology is not yet known. This paper reports the presence of a related cytokine, lymphotoxin, which is produced only by lymphocytes, in the serum of malarial patients. This is the first report of raised serum levels of lymphotoxin in a systemic disease state. When injected into mice, recombinant human lymphotoxin induced hypoglycaemia and increased serum levels of interleukin-6. These changes, which are seen in severe experimental and human malaria, were also provoked by TNF. Both of these cytokines acted synergistically with interleukin-1, which has also been reported to be raised in malaria, to produce these alterations. These observations imply that lymphotoxin, as well as TNF, may contribute to the hypoglycaemia and raised serum interleukin-6 observed in malaria. This reduces the likelihood of effectively blocking the pathology of this disease by the use of neutralizing antibody directed against just one member of this family of functionally overlapping mediators.