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Biomedical subjects

M Kubera

Publications and source records attributed to M Kubera.

At least 37 records · Page 2Linked to original sources
PubMed1996

Effect of hypothalamic lesion or chemical axotomy on restitution of immunoreactivity in mice after cyclophosphamide administration.

Splenocytes harvested from mice that underwent chemical axotomy (by 6-hydroxydopamine) or that had electric lesions in their anterior hypothalami demonstrated a significant decrease in their proliferative ability after concanavalin-A stimulation in vitro. In axotomized mice pre-treated with cyclophosphamide, faster restitution of the proliferative activity was observed on days 6-8 after the drug's administration. Splenocytes isolated from mice treated with 6-hydroxydopamine did not exhibit any suppressive activity, which is characteristic of the restitution period following administration of cyclophosphamide. These results indicate that the autonomic nervous system exert a direct effect on immunoreactivity and on processes which are responsible for restitution after cyclophosphamide-induced immunodisorders.

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PubMed1995

The effect of chronic treatment with imipramine on the immunoreactivity of animals subjected to a chronic mild stress model of depression.

A depression-like state was induced in Wistar rats by chronic (3-week) exposure to very mild, unpredictable stress, which led to diminished food consumption and diminished preference for sweet drinks (anhedonia). Anhedonia was then abolished by 5 weeks of daily administration of imipramine to the continually stressed animals. One day after the last drug injection and stressful event, a statistically significant decrease in the proliferative activity of splenocytes to Con A stimulation in vitro was observed in those animals. Eight weeks of stress (without antidepressant therapy) affected likewise, but in a less potent and non-significant manner, the activity of splenocytes. Administration of imipramine alone for a period of 5 weeks did not modify the activity of these cells.

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PubMed1994

Protective effect of lithium on the stress-induced depression of cell-mediated immunity in mice.

The effect of lithium chloride (LiCl) administration on the stress-induced depression of cell-mediated immunity was studied in mice. Two models of stress-induced depression of immunity were used: (1) keeping the animals at a temperature of 4 degrees C twice for 24 h at a 24-h interval, and (2) keeping them in the dark for 96 h. Both kinds of stress significantly decreased the reactivity of cell donors in the graft-versus-host (GVH) reaction and recipients in the host-versus-graft (HVG) reaction. Treatment with LiCl of the cell donors in GVH reaction or the recipients in HVG reaction daily for three weeks before stress application completely abolished the immunosuppressive effect of "cooling" stress, but not "darkness" stress. The LiCl is thus shown as a potential immunomodulator protecting mice from some forms of the stress-induced depression of cell-mediated immunity.

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PubMed1994

Immunoreactivity of ageing C57BL female mice rendered tolerant to the H-Y antigen.

Transplantation tolerance to the H-Y antigen, induced in neonatal or young adult C57BL female mice, beneficially affected their immunoreactivity during the process of ageing. The tolerance acquired in 2-month-old females significantly increased their splenocyte graft-versus-host (GVH) reactivity and the production of interleukin-2 (IL-2) at the age of 18 months. The neonatally induced tolerance also resulted in a higher weight of the thymus and a significantly enhanced GVH reactivity of thymocytes in 18-month-old females compared to control mice of the same age.

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PubMed1994

Effect of immobilization stress on tumor growth in mice.

The effect of immobilization stress applied daily for 2 h on the development of MF-RSV tumor graft in mice and on survival of the hosts was studied. While a single acute stress applied to mice simultaneously with a transfer of MF-RSV cells stimulated antitumor defense, chronic stress applied both before and/or after tumor cell implantation accelerated the death of recipients. The shortest survival time was found in mice which were stressed for 3 weeks before implantation and on, until their death. Heat shock applied to MF-RSV tumor cells before implantation significantly reduced their growth ability in the hosts.

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PubMed1992

Stress-induced changes in muscarinic and beta-adrenergic binding sites on rat thymocytes and lymphocytes.

This study examined the effect of immobilization stress on the expression of muscarinic and beta-adrenergic receptors on thymocytes and lymphocytes obtained from 5-month-old L-E male rats. After 2 h immobilization (acute stress) there was a significant increase in specific binding of [3H]-DHA to beta-adrenergic receptors on thymocytes and on lymphocytes from the blood but not from the spleen, whereas [3H]-QNB binding to muscarinic receptors in those cells was not altered in comparison with the undisturbed control. Chronic immobilization stress (5 days, for 2 h) decreased the [3H]-QNB binding to lymphocytes collected from the spleen and blood but not from thymus; it caused neither a significant change in the 3H-DHA binding to thymocytes nor lymphocytes obtained from the blood and spleen.

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PubMed1992

Down-regulating effect on cellular immunity of the NSF17 factor produced by murine neonatal spleen cells fused with BW 5147 thymoma cells.

The non-specific factor NSF17 produced by mouse newborn splenocytes fused with BW 5147 thymoma cells was tested in vivo for its immunosuppressive activity. NSF17 administered i.p. in a single dose into adult mice significantly decreased the PHA-induced proliferative response of lymphocytes, regional graft-versus-host reaction, and delayed-type hypersensitivity.

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PubMed1991

The effect of lithium chloride treatment on cell-mediated immunity in mice.

The immunomodulatory effect of lithium chloride (LiCl) administered i.p. to adult mice (150 mg/kg/day) on cellular immunity in vivo was investigated. A short (6-day) treatment with LiCl of either spleen cell donors in semiallogeneic or xenogeneic GVH reaction, or recipients in semiallogeneic HVG reaction, significantly diminished the early sings of local cell-mediated immunity. A short-term LiCl treatment of donor mice also abrogated systemic GVH reaction in newborn F1 recipients, while a treatment prolonged for 20 days did not alter the high GVH response of spleen cells typical for untreated donors. Thus, a striking time-dependent efficacy of LiCl on the reduction of GVH reaction was found.

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PubMed1991

The influence of the age of donors and recipients on the regional graft-versus-host reaction in mice.

Regional graft versus host (GVH) reaction in mice induced by injection of parental strain spleen cells into the footpad of F1, recipients, was measured 7 days later by a popliteal lymph node (PLN) enlargement index. Young, 6-week-old F1 hosts can be used for studying the age- and sex-dependent GVH reactivity of parental strain donors. On the other hand, senescent, 21-24-month-old F1 recipients are able to mount a host versus graft response against parental antigens which may obscure the typical GVH reaction. The PLN enlargement in syngeneic old F1 mice points to an autoimmune mechanism of this phenomenon.

Aging↗
PubMed1989

Effect of neonatal spleen and thymus implants on H-Y incompatible skin grafts.

The transplantation reactivity of adult splenectomized C57BL females to H-Y incompatible skin grafts was significantly reduced by the implantation of spleen and thymus from foetal or 0-1-day-old syngeneic female donors. The thymus implant served as a possible source of natural suppressor cell precursors and the spleen implant as a microenvironment for their maturation.

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PubMed1988

The role of prostaglandin E in the natural suppressor activity of spleen cells from newborn rats.

Spleen cells from newborn to 2-day-old, but not 3-day-old or older, rats suppress the activity of cells from adult animals in xenogeneic local graft-versus-host (GVH) assay. The duration of neonatal suppressor cell activity can be significantly prolonged by treating newborn rats with exogenous prostaglandin E2 (PGE2), and the suppression was completely abolished by administration of PGE inhibitor indomethacin. The results thus demonstrate an involvement of PGE2 in the mechanism of action of neonatal suppressor cells and may explain some discrepancies concerning the nature of natural suppressor cells present in newborn animals.

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PubMedDate not supplied

Modulation of cell-mediated immunity by lithium chloride.

Immunomodulation of cell-mediated immunity was studied in mice treated with either lithium chloride (LiCl), anti-CD8 monoclonal antibody or their combination. While 6-day LiCl treatment decreased the ability of their splenocytes to induce a local graft-versus-host reaction--anti-CD8 abolished this effect. The proliferative response of spleen cells from those three groups of mice to concanavalin A stimulation in vitro was significantly increased. The natural killer (NK) cell toxicity of the mice was decreased by over 43% after the 6-day LiCl treatment, but was x 2.5 higher then the control value after a longer 21-d treatment. These results indicate that the immunomodulatory capacity of lithium is dependent on the type of cell population studied, and on the schedule of administration.

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PubMedDate not supplied

Modulation of neutrophil activity by submandibular gland peptide-T (SGP-T).

The heptapeptide submandibular gland peptide-T (SGP-T; sequence = Thr-Asp-Ile-Phe-Glu-Gly-Gly) was isolated from rat submandibular glands based on its ability to reduce endotoxic hypotension. Since these glands also modulate neutrophil function, the effects of SGP-T on neutrophil function were investigated. I.v. SGP-T (35 and 100 micrograms/kg), when administered prior to and after the s.c. implantation of a carrageenan soaked sponge into rats, significantly reduced the accumulation of neutrophils in the sponge. Neutrophils retrieved from saline soaked sponges generated substantial amounts of superoxide anion in response to both phorbol myristate acetate (PMA) and N-fornyl-methionyl-leucyl-phenylalanine (fMLP), whereas those obtained from carrageenan impregnated sponges were refractory to these oxidative stimuli. Treatment with SGP-T promoted a dose-dependent recovery in the ability of neutrophils obtained from carrageenan soaked sponges to generate superoxide anion. This study, by identifying SGP-T as a regulator of neutrophil function, supports the concept that salivary glands are involved in the regulation of inflammatory responses.

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PubMedDate not supplied

Submandibular gland peptide-T (SGP-T) modulates ventricular function in response to intravenous endotoxin.

A novel peptide hormone isolated from salivary glands, submandibular gland peptide-T (SGP-T), protects against the enhanced hypotensive response to intravenously administered lipopolysaccharide (LPS; 3.5 mg/kg; Salmonella typhosa) in rats with their submandibular glands removed (sialadenectomy). In this study, we examined the effects of SGP-T on LPS-provoked perturbations of heart function. Sialadenectomy did not alter basal heart function, although the sialadenectomized rats exhibited more pronounced reductions in ventricular peak systolic pressure (VPSP), ventricular pressure at max dP/dt (Pmax dP/dt), and maximum ventricular negative dP/dt (-dP/dt) relative to unoperated controls following LPS challenge. These changes were primarily due to changes in afterload (blood pressure). However, in sialadenectomized rats LPS-induced changes in Pmax -dP/dt (ventricular pressure at maximum -dP/dt) did not correlate with changes in VPSP, which suggests that sialadenectomy may alter the systolic component of the heart beat. The peptide SGP-T, at doses of 1 and 3.5 microg/kg, corrected Pmax -dP/dt and all other endotoxin-induced changes in heart function. Since Pmax -dP/dt is a measure of relaxation during diastole, the submandibular glands appear to play a role in protecting the heart against the adverse effects of acute endotoxin administration on ventricular relaxation. These effects of the submandibular glands may be mediated by the release of the peptide SGP-T.

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