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Y Naot

Publications and source records attributed to Y Naot.

54 records · Page 3Linked to original sources
PubMed1979

Mitogenic activity of Mycoplasma pulmonis. I. Stimulation of rat B and T lymphocytes.

The mitogenic activity of Mycoplasma pulmonis towards both rat B and T lymphocytes has been demonstrated. The data summarized in this report show that spleen cells obtained from T X BM rats were extensively activated by M. pulmonis. Furthermore, M. pulmonis has been demonstrated to induce the development of antibody producing cells, as attested by the appearance of direct plaque forming cells against SRBC and TNP-SRBC in spleen cultures exposed to this mitogen. It was also demonstrated that rat thymus cells and a part of the lymph node T-cell population responding to either Con A or PWM, were stimulated by M. pulmonis, the response being weaker than that of rat B-cell populations. It was thus concluded that M. pulmonis activates both rat B and T lymphocytes. This mitogenic stimulation, however, is not equally exerted on both these populations, being strongly effective upon B cells and less so on T cells.

Animals↗
PubMed1979

Histamine levels in ovarian hyperstimulation syndrome.

Ovarian hyperstimulation syndrome was produced in rabbits by administration of human menopausal gonadotropin (hMG) and human chorionic gonadotropin (hCG). Histamine levels in the animals' plasma were determined by an enzymatic-isotopic assay. The results of this study show that there is no statistically significant difference between histamine levels in ovarian hyperstimulated animals as compared with control animals. Furthermore, no differences in the number of mast cells in the ovaries could be demonstrated between the 2 groups. It is concluded that histamine probably does not play a role in the pathogenesis of this syndrome. The relevance of this suggestion to other proposed mechanisms on the etiology of ovarian hyperstimulation syndrome is discussed.

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PubMed1978

Mycoplasma infection in pregnant rats: low viability of foetuses and newborn offspring.

The controversy regarding the possible role of genital mycoplasma infection in human reproductive failure gave rise to a study in which pregnant rats, previously shown to be of normal fertility, were inoculated 7-11 days after conception with either Mycoplasma arthritidis or an equal volume of sterile broth medium. Repeated observations during the course of pregnancy revealed several pathogenic effects. A statistically significant decrease was observed in the mean litter size of infected mothers. Furthermore, the offspring showed low viability at birth and, still more, at 10 days after birth. Our data are compatible with the hypothesis that genital mycoplasma infection plays a role in reproductive failure.

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PubMed1978

Activation of B lymphocytes by mycoplasma mitogen(s).

Various strains of the murine mycoplasma M. neurolyticum have been shown to induce extensive blast transformation of mouse lymphocytes, comparable in strength to mitogenicity exerted by these mycoplasma species on rat lymphocytes. The data summarized in this report demonstrate that this mitogenic effect is non-specific. Lymphoid cells from mycoplasma free, germ-free mice were activated to the same extent as those lymphocytes obtained from conventionally bred animals. Lymph node cell suspensions obtained from athymic nude mice were strongly activated by M. neurolyticum mitogen. Furthermore, mouse thymocytes and mouse T-cell enriched populations, were not stimulated by these mitogens. It was thus suggested that M. neurolyticum activates mouse B lymphocytes.

Animals↗
PubMed1978

Differentiation and activity of mast cells following immunization in cultures of lymph-node cells.

An extensive clonal differentiation into mast cells from primitive blast cell precursors occurred when lymph node cells obtained from mice immunized with horse serum were cultured on mouse embryonic skin monolayers. Horse serum was always present in the culture as a constituent of the nutritional medium. Mast cells developed to lesser extent also in cultures prepared from non-immunized mice. However, a clear difference in mast cell-granule ultrastructure and in histamine content was noted between the two. In cultures of lymph nodes cells from non-immunized mice the granules were tiny and uniform in size and in staining density; whereas granules in the immune cultures were larger and non-uniform in size and in staining density, and the intragranular organization manifested alterations of various forms. The content of intracellular histamine per 10(6) mast cells was about equal in both cultures. However, much more free histamine (per 10(6) mast cells) gradually accumulated in cultures of the immune lymph node cells, indicating higher rates of synthesis and release of histamine. The mast cells were readily degranulated by heat-inactivated (IgG1) sera of the mice used as donors of the lymph node cells. 92% of the mast cells were degranulated and as much as 80% of the histamine was released. The degranulation was accompanied by an immediate (albeit reversible) response of the fibroblast cells in the monolayer. A shift of the well-stretched cytoplasm of the fibroblasts opened numerous 'window' over the whole monolayer. The degranulated mast cells survived the process and could be maintained further in the cultures. Moreover, they were capable of repeated degranulation, releasing 50% of their histamine, even after four degranulation cycles performed over a 7 days' period of culture. No cytotoxic effect on the mast cells was noted and the histamine content in culture, 3 days after degranulation, seemed to be higher than in the undergranulated control cultures--suggesting an intensified rate of histamine synthesis.

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PubMed1977

The modulating effect of human chorionic gonadotropin on lymphocyte blastogenesis.

Human chorionic gonadotropin (HCG) produced by fetal trophoblastic cells was suggested to play a role in the suppression of maternal lymphocyte response against the fetal allograft. Reports supporting this concept have demonstrated a suppressive effect of crude HCG on lymphocyte blastogenesis. However, similar doses of purified hormone preparations were unable to inhibit lymphocyte stimulation with mitogens. A modulating influence of phenol-free and immunoglobulin-free HCG preparation on lymphocyte blastogenesis is presented. Enhanced lymphocyte stimulation with various mitogens occurred in cultures supplemented with HCG at low doses. On the other hand, higher hormone concentration exerted an inhibitory effect on lymphocyte blastogenesis. An increase in lymphoid cell concentrations was demonostrated in cultures supplemented with the hormone preparation. These observations are compatible with the suggested role of HCG in the maternal tolerance toward a histoincompatible fetus.

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PubMed1977

Lymphocyte activation by various Mycoplasma strains and species.

The capacity of various mycoplasma strains and species to induce lymphocyte transformation in vitro was studied. Of six strains of Mycoplasma pulmonis studied, five displayed mitogenic activity with rat lymphocytes. Among those M. pulmonis strains, our MP15 isolate and the Negroni strain exhibited particularly potent mitogenic capacity. The murine mycoplasmas M. neurolyticum and M. arthritidis shared this mitogenicity for rat lymphocytes. However, the human mycoplasmas M. fermentans, M. pneumoniae, M. hominis, M. orale, and Acholeplasma laidlawii did not activate rat lymphocytes. Lymphocytes obtained from germfree rats were activated to the same extent as those from animals bred under conventional conditions. The mitogenic potency exhibited by mycoplasma was not restricted to infective microorganisms, and preparations of killed mycoplasma particles exerted an extensive lymphocyte transformation. The data show that the mitogenic activity of mycoplasmas is not confined to a single mycoplasma isolate and that it acts in a nonspecific manner.

Animals↗
PubMed1973

Role of gene 52 in bacteriophage T4 DNA synthesis.

In an attempt to elucidate the mechanism of delayed DNA synthesis in phage T4, Escherichia coli B cells were infected with H17 (an amber mutant defective in gene 52 possessing a "DNA-delay" phenotype). The fate of (14)C-labeled H17 parental DNA after infection was followed: we could show that this DNA sediments more slowly in neutral sucrose than wild-type DNA 3 min postinfection. In pulse-chase experiments progeny DNA was found to undergo detachment from the membrane at 12 min postinfection. Reattachment to the membrane was found to be related to an increase in rate of DNA synthesis. A nucleolytic activity that is absent from cells infected by wild-type phage and from uninfected cells could be detected in extracts prepared from mutant-infected cells. In contrast, degradation of host DNA was found to be less extensive in am H17 compared with wild-type infected cells. Addition of chloramphenicol to mutant-infected cells 10 min postinfection inhibited the appearance of a nuclease activity on one hand and suppressed the "DNA-delay" phenotype on the other hand. We conclude that the gene 52 product controls the activity of a nuclease in infected cells whose main function may be specific strand nicking in association with DNA replication. This gene product might directly attack both E. coli and phage T4 DNA, or indirectly determine their sensitivity to degradation by another nuclease.

Carbon Isotopes↗
PubMed1971

Role of gene 46 in bacteriophage T4 deoxyribonucleic acid synthesis.

In an attempt to establish whether Escherichia coli B infected with N130 (an amber mutant defective in gene 46) is recombination-deficient, the postinfection fate of (14)C-labeled N130 parental deoxyribonucleic acid (DNA) was followed, its amount in complex with the host cell membrane being determined in sucrose gradients after mild lysis of the infected cells. The parental DNA was found to undergo gradual detachment from the membrane during infection. Pulse-chase experiments similarly showed that newly synthesized DNA is normally attached to the host cell membrane and is detached by endonucleolytic breakage at a late stage of infection. The conclusion is that only attached DNA molecules are replicated by membrane-bound replicase, whereas those detached by endonucleolytic breakage are not. It thus seems that the gene 46 product controls the activity of a nuclease whose main function is recombination of DNA nicked by endonuclease, thereby attaching it to the host cell membrane. The rate of T4 DNA synthesis is apparently governed by the efficiency of recombination. Supporting evidence was found in experiments with the double mutant N130 x N134 (genes 46, 33).

Carbon Isotopes↗
PubMedDate not supplied

Interactions of mycoplasmas with lymphocytes and macrophages.

The effects of interactions between mouse lymphocytes, peritoneal macrophages and Mycoplasma pulmonis mitogens on the growth of infective M. pulmonis in infected cultures were studied. Lymphocytes transformed into blast cells following in vitro exposure to either M. pulmonis mitogens or concanavalin A supported the multiplication of M. pulmonis to a greater extent than did unsensitized lymphocytes. Mitogenic stimulation of lymphocytes by M. pulmonis did not induce the release in vitro of lymphokines capable of enhancing the killing of infective organisms by mouse peritoneal macrophages. In addition, it has been shown that direct interactions of sensitized lymphocytes with macrophages in the presence of M. pulmonis mitogens not only did not enhance phagocytosis of the infecting organisms, but rather provided improved culture conditions for the replication of M. pulmonis as compared to cultures of macrophages with unsensitized lymphocytes or macrophages cultured alone. It can therefore be concluded that mycoplasmastatic or mycoplasmacidic capacities of mouse peritoneal macrophages are not enhanced due to the interactions of macrophages with lymphocytes sensitized by M. pulmonis mitogens.

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PubMedDate not supplied

Role of mitogenicity in pathogenicity of mycoplasmas for murine hosts.

The mitogenicity and pathogenicity of Mycoplasma pulmonis were compared in two rat strains. Both the mitogenic and the pathologic effects induced by M. pulmonis membranes were more severe in Lewis rats than in Hooded rats, and were dependent on the mitogen doses used. It was concluded that the severity of lung lesions induced by M. pulmonis membranes correlated with the degree of mitogenic responses of the different rat strains to this organism. The roles of T- and B-cell mitogens in induction of pneumonia were studied in Hooded rats treated intranasally with either the T-cell mitogen concanavalin A or with M. neurolyticum membranes which stimulate the B-cell populations, or with both concanavalin A and M. neurolyticum. Results clearly showed that the individual B- and T-cell mitogens affected the lungs of treated animals. Nevertheless, the mitogenic co-stimulation of both B and T lymphocytes in rat lungs was necessary to obtain maximal development of interstitial lymphocytic pneumonia.

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PubMedDate not supplied

In vitro studies on the mitogenic activity of mycoplasmal species toward lymphocytes.

The observed mitogenic activity of many mycoplasmal species provided the impetus for studies on this biologic manifestation. Studies designed to define the rat lymphocyte populations activated in vitro by Mycoplasma pulmonis showed that both B and T cells are activated. On the other hand, Mycoplasma neurolyticum induces nonspecific blastogenesis of the B-cell population of both rats and mice. These results and those of other workers suggest that the lymphocyte subpopulations activated by mycoplasmas differ with the mycoplasmal species and the origin of the lymphocytes. Further, one mycoplasmal species activates lymphocytes obtained from different species. Experiments performed to localize and define the biochemical nature of mitogens of M. pulmonis demonstrated that membranous outer-surface proteins are major constituents of the mitogenic factors. Membrane carbohydrates, but not lipids, may also be involved in the mitogenicity of M. pulmonis. Further studies establish a direct correlation between mitogenicity and pathogenicity of M. pulmonis in rats.

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PubMedDate not supplied

Lysis and necrosis: analysis of two cytotoxic phenomena mediated by lymphocytes.

Stimulation of rat lymphocytes by allogeneic and xenogeneic (mouse) embryo fibroblast monolayers or by pokeweed mitogen (PWM) generate two different cytotoxic manifestations: a) cell-mediated target cell lysis obtained by contact between effector cells and target cells; b) cytotoxicity caused by lymphotoxin (here termed "necrosis"). Activation of hypersensitive lymphocytes by soluble antigen, e.g., keyhole limpet hemocyanin (KLH), produces only necrosis but no lytic effect. This difference between mitogen and antigen activation is attributed to the affinity of the mitogens for target cell membranes. There is a marked difference in the time of onset of the two phenomena. Ten minutes after the effector cells have been introduced to the target monolayers, lysis of fibroblasts becomes visible, whereas necrosis usually develops only 48 to 72 h later. A clear difference in the morphology of the two types of target cell killing was seen when the cultures were stained in situ with trypan blue. Lysed target cells produced blebs and underwent fragmentation, scattering cytoplasmic droplets. During a 10-min to 24-h period, these cells excluded the dye. Only much later (after greater than 30 h), when the cell remnants had undergone a further slow "decay" process, did they stain with trypan blue. In cultures rendered necrotic by lymphotoxin, the killed fibroblasts preserved their morphological integrity but the nuclei became markedly stained with trypan blue. Lymphotoxin was found to be effective only in highly concentrated macrophage and fibroblast cultures. In sparsely populated macrophage cultures, the mediator(s) did not effect cell death but nonetheless exerted marked morphological changes. Vacuoles containing lipids developed and eventually occupied the greater volume of the cytoplasm. Giant lipid droplets were seen leaking out of the macrophage cytoplasm. It is suggested that lymphotoxin does not kill directly, but rather that metabolic products released by the vigorously stimulated target cells cause the necrotic effect in the cultures.

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PubMedDate not supplied

Comparison of mitogens from Mycoplasma pulmonis and Mycoplasma neurolyticum.

Studies on Mycoplasma pulmonis and Mycoplasma neurolyticum mitogenesis demonstrated that macrophages are not essential for the interactions of M. neurolyticum with B lymphocytes, whereas M. pulmonis that stimulates B and T lymphocytes depends on macrophages to fully exert its mitogenic effects. Membranes of both species carry the mitogenic as well as pathogenic potentials. However, M. neurolyticum major mitogens are biochemically distinct from those of M. pulmonis. Furthermore, M. pulmonis mitogenesis is directly correlated to the mycoplasmal-induced pathogenic effects, while no such correlation could be established with M. neurolyticum. It was, therefore, concluded that M. pulmonis and M. neurolyticum differ in the biochemical and biological natures of their mitogens.

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