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Biomedical subjects

R B Zurier

Publications and source records attributed to R B Zurier.

At least 73 records · Page 4Linked to original sources
PubMed1984

Analysis of peritoneal macrophages in continuous ambulatory peritoneal dialysis patients.

Peritoneal macrophages (PMC) from patients undergoing continuous ambulatory peritoneal dialysis (CAPD) were compared to peritoneal macrophages from healthy volunteers and to peripheral blood monocytes (PBM) from CAPD patients, hemodialysis patients, and healthy volunteers. PMC from CAPD patients had morphology similar to PMC and PBM from healthy volunteers. HLA-DR antigen and Fc receptors were present on the cell surface. These monocytes had similar sequential morphologic changes in long-term culture compared to PBM from healthy volunteers. Phagocytosis, hydrogen peroxide generation and bactericidal activity were the same in PMC from CAPD patients as in PBM from healthy volunteers. Chemotaxis and eicosanoid precursor uptake studies suggest that PMC from CAPD patients may be relatively immature bone-marrow-derived cells. Although these cells function well as phagocytes, further study is warranted to define their immune competence, many components of which develop during differentiation into mature macrophages and may therefore be deficient in patients undergoing CAPD.

Adolescent↗
PubMed1984

Inhibition of lung fibroblast growth by human lung mononuclear cells.

Mononuclear cell-fibroblast interactions in the normal human lung are poorly understood. To investigate these interactions, we characterized the effect on lung fibroblast growth of supernatants from nonadherent lung mononuclear cells cultured with or without phytohemagglutinin (PHA). Supernatants from unstimulated cells had no effect on fibroblast growth. Supernatants from lung mononuclear cells stimulated by PHA inhibited fibroblast growth in a dose-dependent fashion. This inhibition was mediated by a nondialyzable, noncytotoxic, soluble factor(s) that was partially heat labile and sensitive to digestion with trypsin. Production of this factor(s) was dependent on T-lymphocytes and occurred within 4 h of the initiation of lung mononuclear cell-PHA cultures. Because prostaglandins can mediate mononuclear cell effects on fibroblast growth, we examined the relationship between the inhibition of fibroblast growth caused by PHA-stimulated nonadherent lung mononuclear cells and lung fibroblast prostaglandin production. The nonadherent lung mononuclear cell supernatants stimulated fibroblast PGE2 production, and exogenous PGE2 was capable of inhibiting fibroblast growth. However, the inhibition of fibroblast growth caused by nonadherent lung mononuclear cells stimulated by PHA was not mediated by fibroblast prostaglandin production. Inhibition of lung fibroblast growth by stimulated lung mononuclear cells may be important in regulating fibrosis in the human lung.

Cell Extracts↗
PubMed1984

Oral administration of prostaglandin E2 to humans: effects on peripheral blood leukocyte function.

We examined the effect of small orally administered doses of prostaglandin E2 (0.5 and 1.0 mg) on human peripheral blood leukocyte function. Plasma levels of 13,14-dihydro-15-keto-prostaglandin E2 peaked at 1 hour and returned to baseline at 3 to 4 hours. Adherence of lymphocytes to virus-infected cells was increased significantly 5 hours after ingestion of prostaglandin E2. Increases in adherence were similar to those found when lymphocytes were incubated in vitro with 10(-10) mol/L prostaglandin E2. Thus, this cell-cell interaction is very sensitive to prostaglandin E. Orally administered doses of prostaglandin E2 had only marginal effects on other leukocyte functions (active and total E-rosette formation, lymphocyte proliferation response to mitogen, and monocyte natural cytotoxicity) that are far less sensitive to prostaglandin E in vitro. Prostaglandin E2 clearly has the capacity to influence lymphocyte function when administered orally to normal humans.

Administration, Oral↗
PubMed1984

The cytotoxic effector cells in preparations of adherent mononuclear cells from human peripheral blood.

We have characterized the effector cells present in fresh adherent cell preparations from human peripheral blood that are responsible for the lysis of K562 and IgG antibody-sensitized P815Y target tumor cells. Purified lymphocytes and monocytes, separated from adherent cell preparations by using techniques that utilized light scatter properties and reactivity of the cells with monoclonal antibodies, were used as effectors for the spontaneous and antibody-dependent cytotoxicity. The role of monocytes was also studied at the single cell level. Our results indicate that when a subpopulation of adherent cells that is B73.1+ (NK cells), B44.1- (non-monocyte), with light scatter characteristics of lymphocytes, is removed from the total adherent cell population, the resultant purified monocytes are unable to spontaneously kill K562 target cells. This data suggests that fresh unstimulated adherent cell cytotoxicity against K562 cells is mediated by lymphocyte contamination in these preparations and that the cell responsible for this killing is probably the NK cell. In contrast antibody-dependent cellular cytotoxicity against P815Y target cells is mediated by monocytes and lymphocytes.

Antibodies, Monoclonal↗
PubMed1983

Lymphocyte adherence in multiple sclerosis: lack of virus specificity.

The virus specificity of adherence of peripheral blood mononuclear leukocytes from patients with multiple sclerosis and from age- and sex-matched healthy volunteers to tissue culture cells infected with measles virus, Newcastle disease virus, and vesicular stomatitis virus was studied. Lymphocyte adherence to uninfected cells is uniformly low (5-15% tissue culture cells with greater than 3 lymphocytes adhered). Adherence to cells infected with virus is enhanced 2- to 4-fold in controls and 2- to 10-fold in patients with multiple sclerosis. Virus-specific antigen, antiserum, and receptor, at least in part, inhibited adherence to all cells tested. It is concluded from these studies that increased lymphocyte adherence in multiple sclerosis is not measles virus specific.

Adult↗
PubMed1983

Prostaglandins and the inflammatory response.

Prostaglandins not only mediate the classic signs of inflammation but also help to regulate the function of cellular constituents in an inflammatory reaction. Clinical and experimental evidence of the role of prostaglandins as mediators is highlighted.

Adult↗
PubMed1982

Antinuclear antibodies in multiple sclerosis.

Low levels of antinuclear antibodies (ANAs) were found by indirect immunofluorescence in the serum of patients with multiple sclerosis (MS). Antibodies were found in 22 (81%) of 27 patients with MS and four (20%) of 20 healthy control subjects, with human epithelial (HEp-2) cells as substrate. Antinuclear antibody titers ranged from 8 to 32 in patients with MS and rarely reached above 8 in control subjects. The most common fluorescence patterns produced by MS serums were diffuse, fine speckled, and diffuse with fine-speckled nuclear fluorescence. Large nucleolar speckles and cytoplasmic fine speckles were also seen. Similar, although stronger patterns were seen in control subjects with positive tests for systemic lupus erythematosus. No correlation was found between ANA and antimeasles antibody titers. The presence of a heterogeneous population of circulating antibodies to a variety of nuclear and cytoplasmic antigens lends further support to the concept that altered immune reactivity exists in MS.

Adult↗
PubMed1981

Suppression of acute and chronic inflammation by orally administered prostaglandins.

Oral administration of a stable analog of prostaglandin E1 (PGE1) 15-(S)-15-methyl-prostaglandin E1, can suppress both chronic adjuvant-induced polyarthritis and acute immune complex-induced vasculitis in a dose dependent manner. Histopathologic studies of tibiotarsal joints from rats with adjuvant disease showed suppression of arthritis in animals treated with the PGE1 analog from time of adjuvant challenge. This study represents the first demonstration of suppressed experimental polyarthritis by an orally administered prostaglandin. Suppression of the acute immune complex-induced vasculitis was demonstrated using 15- methyl-PGE1 administered orally 12 hours prior to antigen-antibody challenge. Diminution of tissue injury resulting from immune complex-induced vasculitis is reflected by a decrease in vaso-permeability, indicating suppressed vascular damage in animals treated with prostaglandin. These studies demonstrate the potential use of orally active prostaglandins as an antiinflammatory agent.

Administration, Oral↗
PubMed1981

Adherence of human peripheral blood lymphocytes to virus infected cells: role of the cytoskeleton and prostaglandin E.

Human peripheral blood lymphocytes from patients with multiple sclerosis (MS) form significantly greater numbers of rosettes with virus infected cells than healthy controls. Because increased lymphocyte adherence in MS may be important to the disease process, we have investigated the mechanisms governing lymphocyte adherence in healthy control volunteers. We have previously shown that prostaglandins E1, E2 (PGE2), and dibutyryl cyclic AMP (db cAMP) increase control lymphocyte adherence to MS levels. We now report that colchicine (10(-7) M) and nocodazole (10(-7) M) significantly increased control lymphocyte adherence to measles virus infected human epithelial (HEp-2) cells. Lumicolchicine had no effect. Cytochalasins A, B, C, and D also had no effect on lymphocyte adherence. Colchicine (10(-5) + 10(-7) M) treatment of mononuclear cells enhanced PGE synthesis in tissue culture. Cytochalasins had no effect on PGE synthesis. Thus, microtubules appear important to adherence of lymphocytes to virus infected cells perhaps by virtue of their involvement and/or control of PG biosynthesis.

Cells, Cultured↗
PubMed1980

Treatment of NZB/W ("lupus") mice with 15(S)-15 methyl PGE1.

The F1 hybrid of New Zealand black and New Zealand white mice--the NZB/W mouse--spontaneously develops a disease similar to human systemic lupus erythematosus. Male NZB/W mice with established disease were treated with a stable derivative of prostaglandin E1, 15(S)-15 methyl PGE1 (4 micrograms twice daily) from 7 months of age. The pge analog prolonged survival of these mice: At 14 months 7 of 10 control mice had died, whereas 9 of 10 15(S)-15 methyl PGE1 treated mice remained alive. Thus a dose of 200 micrograms/Kg/day 14(S)-15 methyl PGE1 retards progression of murine lupus.

Alprostadil↗
PubMed1980

Prostaglandins. Their potential in clinical medicine.

The physiologic role of the prostaglandins is complex and not yet defined precisely. Nevertheless, these ubiquitous compounds do appear important to regulation of cell function and host defenses. The therapeutic potential of the prostaglandins seems to be immense, and their use in a wide variety of clinical conditions is just beginning. Whether they will also prove helpful clinically as modulators of the immune response is not clear. It is likely that an appropriate balance of prostaglandin endoperoxides, thromboxanes, prostacyclins, and probably the stable prostaglandins themselves is important to physiologic regulation of many organ systems and of immunologic reactions. Thus, development of drugs that selectively inhibit one or another of the prostaglandins and their allied compounds may prove fruitful in treatment of many diseases, including those associated with disordered immunity and tissue injury. Prostaglandin therapy in such diseases must proceed with caution. In recent studies addition of amantadine to prostaglandin E (PGE) treatment of NZB/W mice not only increased survival of these animals, but prevented development of circulating antibodies to nuclear constituents including native DNA. The results are encouraging, but must be balanced against the observation that deprivation of prostaglandin precursors also prevented nephritis and markedly increased surival of lupus mice. However, prostaglandins might be useful in a disorder whose course is more easily monitored than that of systemic lupus erythematosus: cutaneous vasculitis. The studies in which even oral administration of a PGE1 derivative suppressed immune complex-induced vasculitis (reversed passive Arthus reaction in rat skin) suggest that a trial of PGE1 treatment of cutaneous vasculitis would not be unreasonable.

Adult↗
PubMed1980

Pinocytosis in human synovial cells in vitro. Evidence for enhanced activity in rheumatoid arthritis.

Human synovial tissue cells in monolayer can be shown to take up and digest a soluble protein, horseradish peroxidase (HRP). Uptake of HRP was linear with increasing concentrations of substrate and cell protein and with time for up to 4 h. Low temperature (4 degrees C), and sodium fluoride, an inhibitor of glycolysis were the most effective metabolic inhibitors of endocytosis. In addition, colchicine, an inhibitor of microtubule assembly, and yeast mannan, an inhibitor of mannose-specific receptors, reduced HRP uptake. Synovial cells from patients with rheumatoid arthritis (RSC) demonstrated a statistically significantly higher rate of endocytosis (247 +/- 107 ng HRP/100 micrograms cell protein per 2 h.) than cells from control, nonrheumatoid patients (NSC) (100 +/- 80 ng HRP/100 micrograms cell protein per 2 h). Thus, it is possible to discriminate RSC from NSC by their quantitatively different rates of endocytosis. Digestion of HRP by synovial cells is statistically significant by 6 h after uptake. A faster initial rate of digestion was seen in RSC. Over the first 6--8 h of incubation 42% of the endocytosed HRP was still cell-associated in RSC and 67% remained in NSC cultures. However, by 24 h 20--30% of endocytosed HRP was found in both types of cultures. These results indicate that endocytosed molecules may accumulate more rapidly in RSC and persist within their lysosomes for a longer time than in NSC. The quantitative determination of enhanced endocytosis by RSC compared with NSC suggests that this increased activity may have a role in the pathological function of synovial tissue in rheumatoid arthritis.

Antimetabolites↗