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Biomedical subjects

A I Michael

Publications and source records attributed to A I Michael.

At least 19 recordsLinked to original sources
PubMed1989

The use of cytoenzymological changes in some parasitic protozoa for screening the carcinogenicity of chemicals.

Changes in the Golgi bodies and in hydrolytic enzymes were observed in parasitic ciliates (Nyctotheroides puytoraci) and flagellates (Opalina sudafricana and Protoopalina sp.) after the administration of a single dose of 0.5 mg beta-naphthylamine (BNA) to their host, Bufo regularis. The experiment was carried out during the host's pre-breeding season, from November to February (when only trophozoites are available); the trophozoites were examined 21 days after the injection of BNA. Use of the silver impregnation technique showed an increase in the size of the granular argentophilic Golgi bodies in all three trophozoites after administering BNA to their host. In addition, a larger number of acid phosphatase and nonspecific esterase granules was found in the endoplasm of the three parasites after the injection. The localization of acid phosphatase and nonspecific esterase was found to be similar to the distribution of the Golgi bodies in both the control and the treated preparations. The results could be useful, in that some protozoans could be employed for the quick detection of chemical carcinogenicity if changes in their hydrolytic enzyme content are used as a diagnostic feature.

Animals↗
PubMed1988

Partial characterization of a fibroblast-stimulating factor produced by cloned murine T lymphocytes.

T cells may regulate tissue fibrosis through the elaboration of soluble factors that stimulate fibroblast growth. The authors previously identified a factor produced by cloned Schistosoma mansoni antigen-specific T cells which served as a competence factor for murine fibroblasts. In the present report, they further characterize this fibroblast-stimulating factor (FsF) and differentiate it from a number of other T-cell-derived lymphokine activities. Crude supernatants from concanavalin-activated cloned T cells were fractionated by gel filtration, ion exchange, or reversed-phase high-pressure liquid chromatography. FsF has an apparent molecular weight of 17,000 and could be differentiated from colony-stimulating factor (CSF), interleukin-3 (IL-3), and interferon (IFN) on the basis of chromatographic characteristics. Highly purified or recombinant IL-2, IL-3, CSF, and IFN had no significant effect on fibroblast proliferation. Furthermore, a monoclonal anti-B-cell-stimulating factor-1 antibody only partially blocked the fibroblast proliferation induced by T-cell supernatants.

Animals↗
PubMed1987

In vitro and in vivo evidence that autoimmune reactivity to collagen develops spontaneously in Schistosoma mansoni-infected mice.

Egg-induced granuloma formation in murine schistosomiasis mansoni results from vigorous anti-parasite reaction by activated T cells, macrophages, eosinophils, and fibroblasts. The present study suggests that strain-specific, autoimmune T-cell reactivity directed against host matrix proteins might also contribute to granulomatous hypersensitivity. T cells from infected C57B1/6, but not from CBA or BALB/c mice, proliferative in vitro in response to denatured collagen. T cells from uninfected mice, previously immunized with soluble egg antigen (SEA), did not respond in vitro to collagen. Spleen cells from acutely infected mice, but not chronically infected or uninfected animals, formed granulomas around collagen-coupled polyacrylamide beads in vitro. This response was blocked by anti-collagen antibodies that had no inhibitory effect on in vitro granuloma formation around SEA-coupled beads. In related in vivo studies, granuloma formation was quantitated after iv injection of SEA-, collagen-, or uncoated beads into normal or infected recipients. The mean diameter of lung granulomas induced by collagen-coupled beads in infected mice was significantly greater than the diameter of granulomas around either collagen beads in uninfected mice or uncoated beads in infected mice. these observations indicate that anti-collagen responses develop spontaneously in Schistosoma-infected mice and suggest that such reactivity might play a secondary role in granuloma formation and the pathogenesis of hepatic fibrosis.

Animals↗
PubMed1986

Production of a fibroblast-stimulating factor by Schistosoma mansoni antigen-reactive T cell clones.

Fibrosis in schistosomiasis is the terminal event of a complex pathophysiologic cascade involving interactions between fibroblasts and both host and parasite products. In the present study, the effect of lymphokines produced by cloned Schistosoma mansoni antigen-reactive T cells on the proliferation of murine fibroblasts was investigated. These T cells previously have been shown to proliferate, produce lymphokines, mediate delayed-type hypersensitivity responses, and generate in vitro granulomas in response to soluble egg antigen (SEA). T cells, co-cultured with irradiated antigen-presenting cells and pulsed with SEA, produced levels of fibroblast-stimulating factor (FSF) comparable to equivalent numbers of dispersed hepatic granuloma cells isolated from infected mice. Supernatants of cloned T cells pulsed with Con A (in the absence of macrophages) contained no detectable interleukin 1 activity, but did stimulate fibroblast activation and growth. T cell FSF activity was trypsin-sensitive, was stable at 56 degrees C but not to boiling, and was retained by Con A Sepharose. Activity was associated with HPLC fractions corresponding to an m.w. of 10,000 to 40,000. Neither recombinant interferon-gamma nor affinity-purified interleukin 2 was capable of stimulating fibroblast proliferation. In functional studies, the degree of fibroblast proliferation was related to the length of exposure to the factor. In addition, quiescent fibroblasts were maximally stimulated by T cell FSF only if a second co-factor such as insulin or epidermal growth factor was present. The synergism between T cell FSF and known progression factors suggests that FSF-T may provide a competence signal to fibroblasts. The present results suggest that a direct molecular link may exist between T cells and fibroblasts in schistosomiasis.

Animals↗
PubMed1986

In vitro granuloma formation using defined antigenic nidi.

The in vitro granuloma model provides an excellent tool to study granulomatous hypersensitivity. In our studies of granuloma formation in schistosomiasis, we have demonstrated the utility of the model with respect to analysis of human PBL responses, cloned T cells, purified antigens of the parasite, and regulatory mechanisms. We have also presented data which demonstrate the applicability of this model to other antigenic systems. While the suggestion that this model may be suitable for the study of sarcoidosis may be premature, we would propose that the system may be adapted to screen potentially causative antigens. Furthermore, with the identification of the critical antigen(s), the in vitro granuloma model will facilitate studies at the clinical level.

Animals↗
PubMed1982

Golgi apparatus and acid phosphatase in mammary gland and kidney cells under the influence of diethylstilbestrol (DES).

It is commonly accepted that hormonal disturbances in experimental animals produce pathological changes in several organs namely in mammary glands and kidney. Taking into consideration the close relationship between acid phosphatase and Golgi apparatus, the present study was undertaken, to study the relationship in kidney and mammary gland cells under the influence of DES. The observation indicate, that acid phosphatase and Golgi apparatus were localized in the cytoplasm of mammary gland and kidney cells. It has also been found a parallel change in the activity of acid phosphatase and the degree of development of Golgi apparatus after DES administration.

Acid Phosphatase↗
PubMed1980

Schistosoma haematobium infection in the white mouse--histopathological and histochemical studies.

Mice were infected with 1000 Schistosoma haematobium cercariae (Egyptian strain). Histopathological and histochemical studies were performed on the different organs, during the first four weeks after infection and on the fourth week after oviposition. Pathological changes during early prepatency matched with those in S. mansoni infection. Eggs were laid in aggregates in the colon and liver. They initiated the development of typical granulomatous lesions. Abundant bilharzial pigment and areas of sclerosis were present in both liver and spleen. The heart, kidneys and urinary bladder were pathologically free. Disturbed succinic dehydrogenase and acid phosphatase enzyme levels were detected which point to a derangement in the functions of the cell organelles.

Acid Phosphatase↗
PubMed1979

Indirect immunoperoxidase tests in the diagnosis of schistosomiasis.

An enzymatic technique, immunoperoxidase histochemistry, was applied in the diagnosis of human schistosomiasis. Sera of patients with S. haematobium, S. mansoni and mixed infection, together with control sera, were studied. The test proved easily applicable and gave reliable results particularly with S. mansoni and double infection. The depth of the colour reaction, was then compared with ELISA readings, but there was no relation in the results of the individual cases.

Enzyme-Linked Immunosorbent Assay↗
PubMed1979

Granuloma size in the liver of mice with Schistosoma haematobium infection and Schistosoma mansoni challenge.

Swiss albino mice have been infected with S. haematobium and challenged with S. mansoni. S. haematobium infection in the mouse runs a course more or less parallel to that of S. mansoni infection. Granuloma has reached a maximal size at 135 days post infection and has regressed thereafter. Suppression of S. mansoni granuloma was observed in mice previously infected with S. haematobium. This manifests the presence of cross immunization.

Animals↗