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Y M Ooi

Publications and source records attributed to Y M Ooi.

At least 19 recordsLinked to original sources
PubMed1987

Induction of mouse monocyte-macrophage replication by a mesangial cell-derived factor.

Conditioned media of cultured mouse mesangial cells (possessing microfilaments) were shown to contain a factor that stimulated splenic monocytes-macrophages and blood monocytes to replicate. Replicated cells were shown to express MAC-1 antigen as demonstrated by immunofluorescence with anti-MAC 1 and to possess Fc receptors as evidenced by their capacity to ingest sensitized erythrocytes. Preliminary characterization revealed the following characteristics: by Amicon ultrafiltration, fractions greater than 100,000 daltons were shown to have biologic activity; chromatofocusing of these active fractions revealed a peak of activity associated with fractions having pH 4; heating to 100 degrees C for 10 minutes abolished almost all activity, whereas trypsin treatment was without effect. The observations suggest a mechanism by which mesangial cells may modulate the proliferation of monocytes-macrophages that infiltrate the glomerulus in glomerulonephritis.

Animals↗
PubMed1985

Evidence for an endothelial cell-derived factor which stimulates the growth of human peripheral blood mononuclear cells.

Evidence is provided which demonstrates that conditioned media of cultured endothelial cells derived from human umbilical veins contained a factor which stimulated peripheral blood mononuclear cell [3H]thymidine uptake. A dose-dependent response in peripheral blood mononuclear cell [3H]thymidine uptake was obtained when cells were incubated with increasing concentrations of supernatant of endothelial cell cultures. Studies on temporal kinetics demonstrated that stimulatory activity was evident when mononuclear cells had been incubated with endothelial cell supernatant for 120 hr or more. Preliminary characterization showed the growth immunoregulatory factor to have a molecular weight greater than 100,000 Da.

Cell Division↗
PubMed1985

Evidence for a mouse mesangial cell-derived factor that stimulates lymphocyte proliferation.

The functions of the glomerular mesangium are served by at least two populations of cells--a cell bearing microfilaments that regulates blood flow, and a phagocytic cell bearing Ia determinants and Fc receptors. We provide evidence that mouse mesangial cells (bearing microfilaments) produce a factor(s) that stimulates spleen cell proliferation. The factor(s) appears to act via monocytes/macrophages, since its stimulatory activity is abrogated by prior depletion of the responding mononuclear cell population of monocytes/macrophages. Confirmation of its action on macrophages was documented by experiments that showed that medium from macrophages incubated with mesangial cell supernatant contained greater amounts of a factor that stimulated [3H]thymidine uptake by macrophage-depleted spleen cell populations. By the cothymocyte proliferation assay, it could be shown that mesangial cell supernatant induced splenic macrophage production of interleukin-1-like activity. Preliminary characterization reveals the factor to have a molecular weight greater than 100,000. Thus, a novel function is delineated for this mesangial cell type that appears capable of modulating the local immune response by providing an amplification signal.

Animals↗
PubMed1985

Modulation of mouse mesangial cell proliferation by macrophage products.

Mesangial hypercellularity is usually found in many models of nephritis characterized by monocyte/macrophage infiltration of the glomerulus. In order to examine the mechanism mediating these events, an in vitro model was used to study the effects of macrophage products on mouse mesangial cells, cultured under conditions which would render them relatively quiescent. Under these conditions, macrophage supernatants stimulated the proliferation of the mesangial cells. The stimulatory effect could be shown to be due in part to enhancement of endogenous mesangial cell PGE production. This was demonstrated by experiments which showed that macrophage supernatants stimulated mesangial cell PGE production, that the stimulatory effect of macrophage products was abrogated by pretreatment of mesangial cells with indomethacin, and finally that exogenous PGE2 stimulated mesangial cell proliferation.

Animals↗
PubMed1983

Identification of a monocyte phagocytic defect in a subpopulation of patients with nephritis.

Experimental studies have demonstrated the cardinal role played by the mononuclear phagocyte system in the removal of antigen-antibody complexes. To assess the functional capacity of phagocytes in patients with renal disease, 33 normal subjects, 10 patients with mesangial proliferative glomerulonephritis, 8 patients with membranous nephropathy, and 8 patients with moderately severe chronic renal failure were studied by an in vitro assay, measuring the ability of isolated monocytes to ingest sheep erythrocytes coated with IgG antibody and to phagocytize latex beads. Monocytes from four patients with mesangial proliferative glomerulonephritis and one patient with membranous nephropathy exhibited a subnormal capacity to ingest the antibody-coated erythrocytes. Additionally, monocytes from two of the four patients with mesangial proliferative glomerulonephritis and a defect in ingesting sensitized erythrocytes had a subnormal capacity to phagocytize latex beads. The results are interpreted in the context of a hypothesis which suggests that patients with immune nephritis show various forms of immune deficit.

Animals↗
PubMed1983

Mechanisms of suppression of mouse mesangial cell proliferation by macrophage supernatants.

The monocyte/macrophage has been identified as an effector cell infiltrating the glomerulus in human and experimental nephritis. To clarify the role of the macrophage in this context, an in vitro system was developed in which mouse mesangial cell cultures were maintained. Macrophage supernatants were obtained from peritoneal macrophages harvested from either resident or endotoxin-stimulated C57BL/6J male mice cultured for 24 hr. Incubation of mesangial cell cultures with macrophage supernatants resulted in depression of mesangial cell metabolism as indicated by incorporation of (3H)-thymidine; the effect was more marked when supernatants of endotoxin-treated mice were used. The molecular mechanisms by which suppression was obtained was clarified by experiments fractionating macrophage supernatants by G-100 column chromatography. By this means, two fractions were obtained with different molecular and physiologic properties. One fraction, a molecular size of 14,600 to 29,000 daltons, was shown to mediate the suppressive effect by stimulating endogenous mesangial cell PGE synthesis; additionally, a novel molecular species was identified, which was biologically active at higher concentrations of macrophage supernatants, had a larger molecular size (29,000 to 68,000 daltons), exerted its suppressive effect by an independent mechanism, and accounted for the inability of indomethacin pretreatment of mesangial cells to abrogate completely the suppressive effect of macrophage supernatant at higher concentrations.

Animals↗
PubMed1983

Human mononuclear cell modulation of endothelial cell proliferation.

Endothelial cell proliferation is a histologic characteristic of several forms of nephritis characterized by infiltration of the glomerulus with mononuclear cells. To investigate the mechanism mediating this event, human endothelial cells isolated from umbilical veins and cultured in vitro were incubated with supernatants of cultured human mononuclear cells. Supernatants from mononuclear cells exerted a dose-dependent stimulatory effect on endothelial cell proliferation. The stimulatory effect of supernatant was almost entirely removed by prior depletion of mononuclear cells of monocytes by adherence, suggesting that a monocyte product was responsible for the activity. To investigate the nature of the ligand responsible, partially purified human interleukin I added to endothelial cell cultures was found to stimulate cellular proliferation.

Cell Adhesion↗
PubMed1982

Biosynthesis of membrane factor B by mouse peritoneal macrophages.

The biosynthesis of many of the complement proteins by cells of the monocyte-macrophage series has been established. Studies on these cells using radiolabelled amino acids demonstrated synthesis of precursor proteins (pro-complement), and the native complement protein similar in size to that found in the plasma. However, synthesis of membrane complement proteins has not been demonstrated, although it has been suggested by previous studies using indirect techniques. In particular, there is evidence for the membrane-associated factor B in human lymphocytes. We report here that resident and thioglycollate-stimulated mouse peritoneal macrophages synthesized, in short-term primary cultures membrane factor B of molecular weight (MW) 95,000 and secreted factor B (MW 90,000) as single chain polypeptides. We also found a large single chain polypeptide with an approximate molecular weight of 195,000, which may be the putative factor B precursor.

Animals↗
PubMed1982

Histamine suppresses in vitro synthesis of precursor (pro-C5) of the fifth complement component (C5) by mouse peritoneal macrophages.

Soluble histamine added to mouse peritoneal macrophages in culture suppressed the synthesis of the functional and antigenic complement component C5. Synthesis of intracellular C5 antigen by resident macrophages was suppressed by 16 to 80%, and functional C5 activity by 13.6 to 87.2% at concentrations of histamine ranging from 10(-6) M to 10(-3) M, respectively; secretion of C5 protein was depressed by 18.3 to 85.5% and hemolytic C5 by 8 to 80%. In thioglycollate-stimulated exudates, intracellular synthesis of C5 protein was reduced by 3.3 to 72.3% and functional C5 activity by 7.6 to 73.5% using similar concentrations of histamine; secreted C5 protein was inhibited by 8.9 to 75.7% and functional activity by 4 to 78%. The suppression of C5 activity in resident and thioglycollate-stimulated cultures was dependent on the dose of histamine with maximal suppression occurring at a concentration of 10(-3) M. Experiments in which specific histamine agonists were used confirmed that the action was mediated by the H2 receptor. The inhibition of C5 antigenic protein synthesis paralleled that detected for functional C5. Immunochemical analysis of C5 antigen synthesized under the influence of histamine indicated that suppression of synthesis of pro-C5 was the major mechanism responsible for the depression of C5 produced under these conditions. The inhibitory effects produced by histamine were shown to be mediated by histamine type 2 receptors as indicated by abrogation of the inhibition by cimetidine (H2 antagonist).

Animals↗
PubMed1981

Modification of glomerular immune complex deposition in mice by activation of the reticuloendothelial system.

To determine the effect of activation of the reticuloendothelial system on the localization of immune complexes in the kidney, a model of passive serum sickness nephritis in the mouse was used, with activation of the reticuloendothelial system with Corynebacterium parvum. Groups of mice, control and C. parvum-treated animals, were injected with BSA-125I-anti-BSA complexes containing 3 mg 125I-anti-BSA. Blood was obtained at 5 min, at 3 h, and at 12 h, when the animals were killed. Blood concentrations of BSA-125I-anti-BSA complexes were reduced in C. parvum-treated animals compared with controls. This appeared to be mediated by two effects, increased uptake of complexes in the liver and spleen, and enhanced degradation of immune complexes as measured by TCA-soluble radioactivity. In vitro studies using cultures of peritoneal macrophages also showed enhanced uptake of immune complexes. The amount of immune complexes deposited in the glomeruli of C. parvum-treated animals was reduced as determined by quantitation of radiolabeled material bound to isolated gomeruli and by immunofluorescence techniques. The results of the study emphasize the role of the reticuloendothelial system in the modulation of immune complex localization in the kidney and suggest a potential use of stimulants of the reticuloendothelial system in the therapy of immune complex nephritis.

Animals↗
PubMed1980

Diminished synthesis of immunoglobulin by peripheral lymphocytes of patients with idiopathic membranous glomerulonephropathy.

Some studies of animal models of serum-sickness nephritis have shown that the lesions of membranous nephropathy develop in animals exhibiting a poor antibody response to the administered antigen (if given in constant amounts). It is postulated that patients with idiopathic membranous nephropathy may share a similar characteristic, namely, a diminished capacity to produce sufficient amounts of antibody. To test this hypothesis, we examined the ability of lymphocytes isolated from 11 patients with this disorder to produce immunoglobulin (Ig)G and IgM on stimulation with a polyclonal B-cell activator, pokeweed mitogen. The peripheral blood lymphocytes (2 x 10(6) cells) from 24 normal individuals had geometric mean production rates of 1,779 ng for IgG, and 2,940 ng for IgM after 7 d of culture in the presence of pokeweed mitogen. By contrast, under identical conditions, lymphocytes from the 11 patients with membranous nephropathy produced significantly lower quantities of both immunoglobulins, with geometric mean concentrations of 511 ng for IgG and 439 ng for IgM. When lymphocytes from patients with membranous nephropathy were co-cultured with normal lymphocytes, the production of immunoglobulin by normal lymphocytes was depressed by 22-82%, suggesting that a population of suppressor cells was responsible for this disturbance in B-cell function. By co-culturing normal lymphocytes with patient lymphocytes depleted of either T cells or monocytes, the suppressor cell was identified as a monocyte.

Adolescent↗
PubMed1979

Genetic defect in secretion of complement C5 in mice.

A genetic deficiency of the fifth (C5) component of complement1-3, a serum glycoprotein of molecular weight (MW) 220,000 (ref. 4), has been found in 39% of inbred strains of mice3. Sera of deficient mice lack detectable C5 activity and protein2,3. In addition deficient mice produce antibody to mouse C5 when injected with sera from C5 sufficient (normal) strains. Levy et al.5 showed that somatic cell hybrids between C5 deficient (B10.D2/old line) macrophages and either C5 sufficient (B10.D2/new line) mouse kidney or chicken erythroblasts secreted haemolytically active mouse C5 in vitro. Several possible molecular mechanisms to account for the findings were considered, but insufficient direct data were available to choose among them. We recently reported that mouse (CD.1 strain) peritoneal cells in culture synthesise and secrete a single chain precursor, pro-C5 (MW approximately 210,000), of the two-chain (alpha chain, 125,000 and beta chain 83,000 MW) C5 protein6. Radiolabelled precursor C5 was contained within the cells and was secreted into the tissue culture media. Using similar methods, we now find that C5 deficiency in each of five different mouse strains (AKR, SWR, DBA/2J8 A/HeJ and B10.D2/old line) is due to a failure in secretion of C5 protein and not to a failure in biosynthesis of pro-C5.

Animals↗
PubMed1979

Immunofluorescent localization of fibronectin in the human kidney.

Fibronectin is a glycoprotein shown previously to be present on the surfaces of cells, connective tissue matrices, and in extracellular fluids. Its distribution in the human kidney was evaluated by immunofluorescence methods studying 65 renal biopsies with a variety of pathologic disorders. Fibronectin was found in the mesangium of the normal kidney and increased proportionately in the disease states characterized by mesangial expansion. It was visualized in glomerular capillary loops in some biopsies with membranoproliferative glomerulonephritis, diffuse proliferative glomerulonephritis, and membranous nephropathy. Additionally, fibronectin was detected in glomerular crescents, diabetic nodules, vascular thrombi, glomerular sclerosis, and variably in the interstitium.

Fibronectins↗
PubMed1979

Biosynthesis and post-synthetic modification of a precursor (pro-C5) of the fifth component of mouse complement (C5).

Mouse peritoneal macrophages synthesized and secreted a precursor (pro-C5) of the fifth component of serum complement (C5) in short-term tissue culture. Approximately 0.2% of the newly synthesized intracellular protein and 0.8% of secreted protein were precipitable with antiserum to mouse C5. The precursor is similar in size to the native serum protein (210,000 daltons), but consists of a single polypeptide chain. In contrast, serum C5 consists of two polypeptide chains (m.w. 125,000 and 83,000) linked by disulfide bridges. An electrophoretic variant of pro-C5 distinct from intracellular C5 was detected in medium from macrophage cultures.

Animals↗