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Biomedical subjects

H Friedman

Publications and source records attributed to H Friedman.

At least 343 records · Page 19Linked to original sources
PubMed1984

Immunostimulation by Legionella pneumophila antigen preparations in vivo and in vitro.

Injection of Legionella pneumophila antigen, either killed vaccine or soluble sonicate thereof, resulted in an enhanced antibody response by mouse spleen cells to sheep erythrocytes as determined by the hemolytic plaque assay. Enhancement was dose dependent and reached a peak response at a concentration of 10(7) bacteria or 50 micrograms of sonicate per animal. Larger doses of antigen were less stimulatory or even depressed the antibody response. Similar enhancement of antibody formation by normal spleen cell cultures to sheep erythrocytes in vitro occurred in the presence of graded amounts of L. pneumophila vaccine or sonicate. In addition, the L. pneumophila antigen stimulated enhanced background antibody formation in vitro in the absence of sheep erythrocytes or specific antigen. It appeared likely that the immunoenhancing activity of the L. pneumophila extract may be unrelated to the presence of lipopolysaccharide since boiling the antigen preparation eliminated much of the antibody-enhancing properties of the extract. A large-molecular-weight surface component from L. pneumophila was also immunomodulatory in vitro. Immunostimulation appeared to be related to effects on macrophages since adherent spleen cell populations rich in macrophages, when derived from spleen cell suspensions incubated with L. pneumophila antigen in vitro, stimulated enhanced antibody formation by normal mouse spleen cells in coculture experiments. Further investigations concerning the mechanism of immunomodulation by L. pneumophila antigen in vivo and in vitro appear to be warranted.

Animals↗
PubMed1984

Relative potency of virulent versus avirulent Legionella pneumophila for induction of cell-mediated immunity.

Guinea pigs were infected with either high-passage, low-virulence Legionella pneumophila or low-passage, high-virulence organisms. On an infectious dosage basis, the high-virulence organisms were much more effective at sensitizing animals for positive skin test responses and splenic lymphocyte proliferation responses to homologous antigens. These results suggest that exposure to low doses of virulent L. pneumophila can effectively prime animals for cell-mediated immune responses.

Animals↗
PubMed1984

Lymphoid cell blastogenesis as an in vitro indicator of cellular immunity to Legionella pneumophila antigens.

The lymphocyte blastogenic transformation assay was adapted to study responsiveness of lymphoid cells from animals and humans to Legionella pneumophila antigens in vitro. Spleen cells from guinea pigs after active immunization with Legionella vaccine, but not from normal animals, responded by blast cell transformation when stimulated in vitro with killed Legionella whole-cell vaccine, sonic extracts thereof, or a purified somatic antigen. The response was dose dependent. Similar lymphocyte blastogenesis occurred with spleen cells from mice sensitized to Legionella by sublethal infection with the bacteria. In addition, blastogenesis occurred with peripheral blood leukocytes from human volunteers tested in vitro with whole-cell vaccine, sonic extracts, or purified somatic antigen. Maximum responsiveness generally occurred 4 to 5 days after stimulation of human peripheral blood leukocytes, but a day or two earlier with spleen cells from normal or sensitized mice. Guinea pig spleen cells generally showed peak responses at the same time as human peripheral blood leukocytes after stimulation in vitro. Blastogenic responses with purified antigen were comparable to those with the whole-cell vaccine or sonic extract. Such antigens from Legionella provide a useful material for inducing responses in vitro as a correlate of cellular immunity to these bacteria.

Animals↗
PubMed1984

Dexamethasone inhibition of DMSO-induced transglutaminase activity and differentiation of leukemic cells.

Treatment of the Friend erythroleukemic (FL) cell line GM979 with dimethyl sulfoxide (DMSO) or n-butyric acid induced erythroid differentiation. Transglutaminase (TGase) activity also increased in these treated cells. Glucocortical steroids, i.e., dexamethasone (DEX) and triamcinolone acetonide, when added to the cultured medium, inhibited the DMSO-induced hemoglobin synthesis but not n-butyric acid-induced hemoglobin synthesis. Similarly, these steroids inhibited DMSO-increased TGase activity but not n-butyric acid-increased TGase activity in intact FL cells. Neither the differentiation-inducing agents nor the steroids had any effect on TGase activity when they were directly added to cell lysates. These results support the view that the increase of TGase activity may be related to erythroid differentiation of FL cells and of its possible role of this enzyme in FL cell-induced differentiation.

Animals↗
PubMed1984

Dimethyl sulfoxide-induced inhibition of the immunosuppressive activity of cultured Friend erythroleukemia cells.

Two Friend leukemia virus-induced tumor cell lines lost their immunosuppressive properties in vitro when treated with dimethyl sulfoxide (DMSO), a known cellular differentiation agent. Incubation of the cell lines, GM 979 and GM 86, with DMSO for 4 days or longer, inhibited their ability to suppress the antibody forming capacity of normal murine spleen cells immunized in vitro with sheep red blood cells. Suppression of the inhibitory capability of the tumor cell lines by DMSO was time dependent. Three days incubation caused only slight, if any, inhibition, while a shorter period of treatment had no effect. Inhibition of the immunosuppressive properties of the tumor cell lines was not due to a decrease in tumor cell viability. The development of previously reported metabolic alterations in the treated cells, such as increased hemoglobin synthesis and other physicochemical alterations, paralleled cellular differentiation, and loss of immunosuppressive properties.

Animals↗
PubMed1984

Muramyl dipeptide-induced enhancement of phagocytosis of antibiotic pretreated Escherichia coli by macrophages.

Treatment of mice with muramyl dipeptide, a known immunoadjuvant, resulted in marked augmentation of the phagocytic activity of peritoneal macrophages incubated in vitro with Escherichia coli. Even greater phagocytosis occurred when the E. coli were pretreated for 2 hr with subinhibitory concentrations of the semisynthetic penicillins cyclacillin or ampicillin, but not penicillin G to which they were resistant. The antibiotic-pretreated E. coli were more rapidly ingested by the macrophages derived from MDP-treated mice as compared to similar cells from normal mice. Optimum augmentation of phagocytosis of untreated or antibiotic-pretreated E. coli occurred 2 to 3 days after administration of MDP to the mice. Similar augmentation of phagocytosis occurred by treating cultures of peritoneal macrophages from normal mice in vitro with MDP prior to incubation with the antibiotic-pretreated bacteria. These results indicate that macrophages from MDP stimulated mice interact with antibiotic-pretreated bacteria to a greater extent than with untreated E. coli, resulting in increased phagocytosis and killing of the bacteria.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1984

Lymphoblastoid cell-induced suppression of human peripheral blood leukocyte mitogenic responses.

Two lymphoblastoid tumor cell lines, the Burkitt lymphoma derived BJAB cell line which is free of Epstein-Barr virus (EBV) and B95-8 cells, which are marmoset lymphocytes transformed by EBV isolated from an infectious mononucleosis patient, were studied in regards to their effects on the blastogenic responsiveness of normal human peripheral blood leukocytes stimulated in vitro with mitogens. Mitomycin C treated tumor cell suspensions, when cocultured with normal human blood leukocytes, markedly depressed the expected blastogenic responses in vitro to concanavalin A, pokeweed mitogen, and phytohemagglutin. In addition, cell-free sonicates from the cell lines also depressed blastogenic responsiveness of the leukocytes in vitro. Heating the sonicates for 10 min at 100 degrees C markedly diminished the suppressive properties of the sonicates, as did ultraviolet light irradiation. The suppressive activity of the B95-8 sonicates was pelleted by high speed centrifugation as compared to the activity of sonicates derived from the BJAB cells. Further studies are warranted to determine the nature and mechanism of suppression of blastogenic responsiveness of normal human leukocytes by soluble components derived from such lymphoblastoid cell lines.

Animals↗
PubMed1984

Suppression of natural killer cell activity by Friend murine leukemia virus.

BALB/c mice infected with Friend murine leukemia virus (F-MuLV) evinced a decreased natural killer (NK) cell activity to susceptible target cells. This suppression increased as the interval between infection and assay was lengthened. The decrease in NK activity due to F-MuLV infection was partially reversible when spleen cells were pretreated with interferon before the cytolytic assay. The ability of F-MuLV-infected splenocytes to bind to target cells was unaltered, indicating that the defect was in the lytic phase of NK cytolysis. When mixed with uninfected spleen cells, F-MuLV-infected splenocytes suppressed their NK cell activity. This suppression was associated with a nylon wool-adherent cell population in the F-MuLV-infected spleens.

Animals↗
PubMed1983

Continuous electrocardiographic monitoring in patients with sickle-cell anemia during pain crisis.

Electrocardiographic studies in patients with sickle-cell anemia have been performed during the normal resting state with routine twelve-lead ECGs. We studied 30 patients with sickle-cell disease in acute crisis with 24-hour continuous electrocardiographic monitoring. The standard ECG demonstrated a high incidence of abnormalities, but only three patients had arrhythmias. These findings contrasted sharply with the results of continuous monitoring, during which arrhythmias were detected in 24 of 30 patients. They were fairly evenly split between atrial (60%) and ventricular (67%). Nine of the patients had "complex arrhythmias" including two with episodes of ventricular tachycardia. Seventeen patients subsequently underwent equilibrium gated-blood pool scans. Eight patients had abnormal contractility and tended to have more arrhythmias on monitoring than those with normal contractility. Thus, continuous electrocardiographic monitoring of sickle-cell patients during crisis revealed a higher incidence of arrhythmias than previously thought.

Adolescent↗
PubMed1983

Cell-mediated immune injury to the heart.

A micro in vitro procedure was utilized to assess cell-mediated immunity of patients following myocardial infarction or cardiac surgery. For this purpose, peripheral blood leukocytes from patients were tested in a microdroplet assay with antigen preparations derived from human cardiac tissue. Whereas whole saline extract and human myoglobin preparations had little effect on the migration of peripheral blood leukocytes in vitro, mitochondrial preparations were markedly effective in inhibiting migration of the leukocytes in the presence of mitochondrial extracts appeared to reflect development of cell mediated immunity to heart antigens after the myocardial infarct or surgery. These results extend the observations that humoral antibody may appear in patient following cardiac injury. The role of either antibody or sensitized lymphoid cells in mediation of post-myocardial infarction or post-cardiotomy syndromes is not clear, but it appears clear that injury to the heart induced auto-reactive responses which may play a role in subsequent pathologic events following the initial cardiac injury.

Adolescent↗
PubMed1983

Influence of viruses on cells of the immune response system.

A wide variety of immune parameters may be influenced in vivo and in vitro during virus infections. Some viruses appear to specifically alter macrophage activity, while other viruses preferentially affect activity of lymphocytes, both B and T cells. There are many mechanisms involved in immune derangement during virus infection, including the possibility that viruses preferentially interact with selected classes of immunocompetent cells. Alternately, some of the events associated with viral derangement of the immune response may be associated with the release or formation of factors by cells infected with a virus which affects other cells of the immune system. Similarly, the development of immune complexes resulting from the interaction of viruses or their components with antibody directed to the virus may influence the immune response, as well as induce other immunopathologic manifestations. Many model systems have been studied, especially those with viruses important to human infection. It is noteworthy that leukemia viruses and, in some cases, other tumor associated viruses may directly alter the immune response, usually before other manifestations of the tumorigenic process is evident. Tumor virus-induced immunomodulation is associated with direct effects of a virus on immunocompetent cells per se as well as the formation of soluble factors induced by the virus infection. These and other considerations indicate that interactions of viruses with the host immune defense system are an important consideration in understanding how virus infection is initiated and progresses, and how such infection affects the host's physiologic activity, including immunocompetence, per se.

Animals↗
PubMed1983

Immunomodulation by small molecular weight bacterial products.

Microbial products are known immunomodulators. Endotoxins derived from gram negative bacteria both enhance and suppress a wide variety of immune responses in vivo and in vitro, depending upon dose, concentration, form, and time of exposure. Studies in this laboratory have shown that a small molecular weight polysaccharide derivative from endotoxin has strong immunomodulatory effects, both in vivo and in vitro, similar to intact LPS. Injection of PS into mice or addition to normal mouse spleen cell cultures results in enhanced responses similar to that observed with LPS as well as with lipoteichoic acid derived from gram positive bacteria. The immunomodulatory activity, both in vivo and in vitro, was related to development of soluble serum factors, most likely interleukins. Similar soluble mediators were observed in vivo since post endotoxin or post LTA serum, when added in small quantities to normal mouse spleen cell cultures, mediated enhanced antibody responses. Normal spleen cell cultures exposed to these materials also released soluble mediators into the supernatants which enhanced the antibody response of normal spleen cell cultures. These observations support the view that similar to larger molecular weight cell wall components, small molecular weight substances such as polysaccharide derivatives, despite lack of toxicity share related mechanisms of enhancing immune responses.

Adjuvants, Immunologic↗
PubMed1983

Role of antibody response helper factors in immunosuppressive effects of friend leukemia virus.

The primary antibody response of BALB/c splenocytes to sheep erythrocytes in vitro was suppressed by infection with Friend leukemia virus (FLV), with the response capacity decreasing with increasing duration of infection. The acquisition of normal antibody responses was amplified by macrophage-produced antibody response helper factor(s). FLV-infected mice were treated with bacterial lipopolysaccharide to induce the release of these helper factors into the serum. Similar to the loss of antibody response capacity by their splenocytes, the FLV-infected mice progressively lost the ability to produce helper factors in response to lipopolysaccharide. In vitro cultures of FLV-infected cells also showed a depressed ability to produce helper factor activity both spontaneously and in response to lipopolysaccharide stimulation. The reconstitution of normal levels of exogenous helper factors to FLV-infected splenocytes restored the antibody response to normal or even elevated levels. These studies indicate that the mechanism for suppression of antibody responses by FLV involves the depression of antibody response helper factor production.

Animals↗
PubMed1983

Cellular immunity to Legionella pneumophila in guinea pigs assessed by direct and indirect migration inhibition reactions in vitro.

Spleen cell cultures from guinea pigs given legionella pneumophila vaccine in complete Freund adjuvant or as a sublethal infection were inhibited in their migration activity in vitro when incubated with specific antigen. Both direct and indirect migration inhibition assays revealed sensitization of the guinea pigs to the bacterium, with demonstrable reactivity 25 to 40 days or more after sensitization. No consistent reactions occurred when the guinea pigs were given the killed Legionella vaccine in incomplete Freund adjuvant in saline. However, spleen cells from guinea pigs injected with sublethal doses of the Legionella vaccine 3 to 4 weeks earlier showed positive migration inhibition factor reactivity. Cutaneous hypersensitivity and lymphocyte blastogenic responsiveness in vitro also developed in guinea pigs sensitized with killed Legionella vaccine in complete adjuvant or given a sublethal infection with the bacterium. These results indicate that in vitro assays for migration inhibitory activity may be utilized to monitor the development of the sensitization of guinea pigs to L. pneumophila, and such reactions correlate with skin reactivity and in vitro lymphocyte blastogenic responses.

Animals↗
PubMed1983

Legionella pneumophila-induced suppression of macrophage spreading in vitro.

Incubation of normal mouse resident peritoneal cell suspensions rich in macrophages with Legionella pneumophila whole cell vaccine or soluble preparations thereof resulted in marked inhibition of the ability of the cells to spread on glass surfaces during a 24-h period. This inhibition, however, was transient in that by day 2 to 3 after culture initiation only partial inhibition was evident, and by day 4 to 5 thereafter most of the treated macrophage cultures showed normal spreading activity. Suppression of macrophage spreading was evident not only with intact Legionella preparations and the sonic extract but also with a lipopolysaccharide-rich somatic antigen preparation and flagella. The suppressive effects of Legionella preparations on a functional activity of normal macrophages in vitro indicate that these bacteria may have a detrimental effect on an important activity of cells involved in the immune defense system.

Animals↗
PubMed1983

Differential complement activation and susceptibility to human serum bactericidal action by Vibrio species.

The ability of Vibrio vulnificus to resist human serum bactericidal action and to activate human complement was compared with similar cultures of Vibrio cholerae and Vibrio parahaemolyticus. Both V. vulnificus and V. parahaemolyticus had similar survival rates in sera and were much more resistant to killing than was V. cholerae. In contrast, V. vulnificus activated significantly less serum complement than did V. cholerae and V. parahaemolyticus. The relative ability of V. vulnificus to survive in serum and activate less complement than other Vibrio spp. tested may be related to its ability to cause chronic tissue infections and septicemias.

Blood Bactericidal Activity↗