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Biomedical subjects

V Lackovic

Publications and source records attributed to V Lackovic.

At least 19 recordsLinked to original sources
PubMed1990

A comparison of regulatory cells in spinal fluid and blood in patients with multiple sclerosis and other neurologic diseases.

Multiple sclerosis is a disease in which immune abnormalities are present both in the CNS and peripheral blood. Whether these changes are primary or secondary to the disease process is not known. We tested T-cell clones derived from activated lymphocytes in the blood and CSF of MS patients and controls for their capacity to regulate T-cell responses to alloantigens. A wide spectrum of regulatory functions were observed, ranging from marked enhancement to almost complete suppression. Clones from different patient populations and anatomic sites were equivalent in their regulatory functions with the net effect of clones in each compartment being suppression. However, certain clones from CSF and peripheral blood had the capacity to stimulate autologous T cells. Percentages of such clones in the peripheral blood of MS patients were significantly higher than in controls, while percentages in MS and other neurologic diseases (OND) CSF were equivalent. Our data suggest that (1) functional suppressor cells are not lost from the blood or CSF or MS and OND patients, (2) lymphocytes that have entered the CNS in patients with MS and other CNS diseases have equivalent regulatory functions, (3) MS may be an illness in which peripheral immunologic events are important in perpetuating the disease process, and (4) responses to autologous antigens may also play a role in this perpetuation.

Adult↗
PubMed1990

[Immunobiologic properties of lactobacilli].

The authors investigated in experiments on mice immunobiological properties of selected strains of lactobacilli (Lbc. acidophilus, Lbc. casei and Lbc. delbruecki). Their immunostimulating action was evaluated from the migrating capacity of lymphocytes into the interepithelial spaces and lamina propria mucosae of the gut. The most marked changes were observed in the group of animals to whom Lbc. acidophilus and Lbc. casei was administered for two weeks by a gastric tube. The protective properties of lactobacilli on the course and development of model infections (virus of encephalomyocarditis) was greatest in mice given Lbc. casei and Lbc. acidophilus by the intraperitoneal route four days before infection. At the end of the two-week period in the Lbc. casei group 66% mice survived and in the Lbc. acidophilus group 34%. The ability of lactobacilli to influence the interferon producing activity was investigated in vitro on a model of peritoneal cells obtained from premedicated mice. The lactobacilli strains themselves did not have interferon inducing properties. However, when the interferon producing capacity of peritoneal cells was assessed after administration of the viral inducer (virus of Newcastle disease) the capacity was much higher, when compared with controls.

Adjuvants, Immunologic↗
PubMed1989

Blood-brain barrier permeability changes during acute allergic encephalomyelitis induced in the guinea pig.

Blood-brain barrier permeability to homologous serum 125I-IgG and to D-[3H]mannitol was studied by means of the brain vascular perfusion method in guinea pigs with experimental allergic encephalomyelitis (EAE). EAE was induced with homologous myelin basic protein (MBP) after pretreatment with foreign protein and muramyl dipeptide (MDP). The results suggest a significant comparable increase in IgG blood-to-brain clearance in the parietal cortex, hippocampus, and caudate nucleus, during vascular perfusion of the brains of animals, after 7 and 20 days of EAE. On the other hand, unidirectional transfer of mannitol in the same period of EAE was markedly augmented only in the hippocampus, but no significant changes in the parietal cortex or caudate nucleus were observed. Cerebrospinal fluid (CSF)/serum ratios for IgG and albumin were both significantly increased, suggesting an increase in blood-CSF barrier permeability, but more for albumin than for IgG. The results were confirmed by immunohistochemical determination of the IgG deposits in the brains of EAE animals, during vascular perfusion with unlabeled homologous IgG. An important role of the blood-brain barrier for the central nervous system immunoglobulin homeostasis during EAE is suggested.

Animals↗
PubMed1989

Human acid- and thermolabile alpha-interferon-like substance: selective reactivity with a monoclonal antibody.

An acid- and thermolabile alpha-interferon-like substance, designated AL-IFN-alpha, has been found in non-processed normal human leukocyte IFN preparations as well as sera from patients with autoimmune or other chronic diseases. Little is known about origin, production and biological activity of these IFN activities. Monoclonal antibodies were obtained which proved highly selective in neutralizing AL-IFN-alpha in both anti-proliferative and antiviral tests. While the monoclonal antibodies were strict specific, polyclonal antibodies against various interferons showed less specificity in these tests. The results suggest that AL-IFN-alpha represents an antigenically distinct IFN-alpha subtype or, alternatively, a new lymphokine with antiproliferative and antiviral activity.

Acids↗
PubMed1989

Abnormal macrophages and NK cell cytotoxicity in human systemic lupus erythematosus and the role of interferon and serum factors.

Macrophage (MO) and natural killer (NK) cell mediated cytotoxicity to K562 target cells were strikingly decreased in patients with systemic lupus erythematosus (SLE). SLE NK cells failed to release soluble factor(s) for lysing the targets. IFN-induced enhancement of both types of cytotoxicity was impaired. NK cells from healthy subjects kept their activity in culture with or without IFN for more than six days whereas SLE NK cell activity declined to zero at day 3. So, the increased IFN level of many SLE patients and a possible prior IFN priming effect seemed unrelated to the insensitivity to exogenous IFN in vitro. Inhibition factor(s) of SLE serum suppressed NK cytotoxicity in the presence of IFN whereas IFN sensitivity of MO remained unaffected indicating the complex regulation by serum components of immune reactions.

Chromium Radioisotopes↗
PubMed1989

Monoclonal antibodies neutralizing human leukocyte acid- and thermolabile interferon alpha.

Using a high titred human leukocyte IFN alpha preparation which contained both acid- and thermolabile (AL-IFN alpha) and acid- and thermostable IFN alpha species in 9:1 proportion for immunization of BALB/c mice, five hybridomas secreting monoclonal antibodies that reacted with AL-IFN alpha were obtained. In antiviral and antiproliferative tests on HL-60 cells, their products showed high degree of specificity for AL-IFN alpha. The results suggest that both the "normal" leukocyte AL-IFN alpha and the IFN alpha found in sera of autoimmune and other chronic patients might belong to the same subtype of IFN alpha.

Animals↗
PubMed1988

Activation of NK cells in subjects exposed to mild hyper- or hypothermic load.

The effect of mild hyper- and hypothermic stress on release of selected hormones (somatotropin, noradrenaline, etc.), interferon (IFN), and activity of NK cells in the blood was examined in groups of young males during a 30 min exposure to 39 degrees C and 4 degrees C. A quick release of somatotropin was registered in 44% of examinees in the hyperthermic group, while the persons exposed to 4 degrees C reacted with a release of noradrenaline only. Concurrently, an elevation of NK cell activity was observed both in the subgroup releasing somatotropin after hyperthermic stress and in the group exposed to cold. Since these forms of mild stress did not lead to an appearance of IFN in the serum, the possibility of an NK cell activating effect of somatotropin and/or the adrenal hormones was tested. While the adrenal hormones stimulated the NK cell activity in vitro, no support for a similar role for somatotropin was found.

Adult↗
PubMed1986

Combined effects of interferon and mutagens on survival of mouse L929 cells.

We studied the effect of mouse interferon (IFN) alpha/beta on the sensitivity of L929 cells to cytotoxic activity of ultraviolet (UV) irradiation or ethyl methanesulfonate (EMS) administration. Exposure of L929 cells to IFN for 48 h before mutagen treatment markedly enhanced their sensitivity to UV, but only slightly to EMS. Incubation of L929 cells after UV-irradiation for 24 h in the presence of low concentrations of IFN (15 units/ml) increased the cellular recovery, while with graded concentrations of IFN the protective activity was inhibited (60 units/ml) and after 250 units/ml the ability of IFN treated cells to recover was found to decrease. Incubation of cells after EMS treatment for 24 h with low (15 units/ml) or moderate (60 units/ml) IFN concentrations markedly reduced the cellular recovery. It has been shown that the extent and the direction of IFN activity on cellular sensitivity to mutagens was influenced by the type of mutagen, IFN-concentration and length of its action on the cell and upon application of IFN before or after mutagen treatment.

Cell Survival↗
PubMed1986

Early intrathecal production of specific IgM and IgG antibodies and alpha-interferon in herpes simplex virus encephalitis.

A complex approach was used in order to establish non-invasively the aetiology in three cases of encephalitis presumptively caused by herpes simplex virus (HSV). As indicative of brain HSV infection was considered the lowered serum to cerebrospinal fluid specific antibody ratio, which also assessed the humoral immune response within the CNS. For this purpose, during ongoing brain tissue infection, the early intrathecal (ITH) production of IgG and IgM antibodies was analysed by a differential enzyme-linked immunosorbent assay (ELISA) along with changing levels of complement-fixing (CF) antibodies in the serum and cerebrospinal fluid (CSF). Antiviral antibody (AA) response was markedly preceded by the appearance of alpha-interferon (IFN) in the serum and CSF. From the CNS biopsy and autopsy specimens one HSV-1 and one HSV-2 strain were recovered.

Adolescent↗
PubMed1984

Clinical and immunological characterization of systemic lupus erythematosus in patients with circulating interferon and migration inhibitory factor.

The simultaneous occurrence of interferon and migration inhibitory factor was found in sera from 9 patients with systemic lupus erythematosus (SLE). Their clinical picture was characterized by a moderate course of the disease. In 7 patients the inflammatory tendoarticular manifestations were accentuated. Glomerulonephritis was found only in 3 patients and was successfully suppressed by immunosuppressive therapy. In the peripheral blood of most of these patients, normal or moderately increased levels of active E-rosettes were found. Therefore we consider these SLE patients as a group with characteristic signs of activated cell-mediated immunity (lymphokine release, active E-rosettes). Although the reason for this activation remains unknown, we suppose that some concomitant bacterial infection, perhaps mycobacterial, may contribute to this immunological phenomenon.

Adult↗
PubMed1982

Production of interferon and other lymphokines during murine tumour growth. III. Characterization of microbial growth inhibitory activity in cell-free supernatants of rat Zajdela ascites hepatoma.

A microbial growth inhibitory factor (MGIF) detected in the cell-free fluid of Zajdela ascites hepatoma of the rat was characterized by means of gel filtration, ion exchange chromatography and isoelectric focusing. It was shown that MGIF is a nondialysable protein with a molecular weight of about 19,000 to 25,000. Charge heterogeneity was revealed by isoelectric focusing which demonstrated pI of 3.8--4.5 and 5.0--6.0. MGIF seems to differ from tumour cell-derived MIF detected in the same ascitic fluids.

Ammonium Sulfate↗
PubMed1981

Accelerated appearance of an ascitic tumour after long-term application of interferon to NZB/W mice.

In two similarly designed experiments female NZB/W mice treated with mouse L-cell interferon developed an ascitic tumour when the treatment was begun at 3.5 months of age. But no tumour appeared within a 6 months' observation period when 6 months old mice were used. A transient rise of anti-DNA antibodies preceded the tumour appearance in mice. The ascitic tumour was sensitive to antimetabolites and insensitive, or marginally sensitive, to alkylating agents or interferon. The tumour cells were adapted to growth in suspension in vitro. They caused tumour growth in various inbred and random-bred mouse lines. Attempts to transfer the tumour to Swiss mice with cell free preparations were unsuccessful.

Animals↗
PubMed1980

The cell growth inhibitory and antiviral effects of interferon in cloned transformed mouse cells.

Eight clones and two subclones of SV40- and seven clones and one subclone of 20-methylcholanthrene-transformed C3H mouse embryonic fibroblasts were compared in tests for sensitivity to the antiviral and cell-growth inhibitory activities of a partially purified mouse L-cell interferon. While the sensitivity of clones and subclones to the antiviral activity of interferon was comparable to that of parent lines, the cell-growth inhibitory activity of interferon in the SV40 clones showed more than 100-fold variation and the methylcholanthrene-transformed cells could be divided into two groups in this respect. No correlation of sensitivity to the cell-growth inhibitory effect of interferon with the chromosome number, interferon-producing capacity or tumorigenicity of the clones could be detected. However, the cells of the interferon-sensitive clones No. 36 of the methylcholanthrene-transformed line were destroyed by macrophages at higher percentage binding of 125I-labeled soybean lectin. These results suggest that (1) the cell-growth inhibitory effect of interferon might be mediated by a specific type of receptors, and (2) N-acetyl-galactosamine present on the surface of interferon-resistant cells in a higher concentration than on interferon-sensitive cells hinders the recognition of cells both by macrophages and by interferon.

Animals↗