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R Sullivan

Publications and source records attributed to R Sullivan.

At least 145 records · Page 8Linked to original sources

The kinetics of the production of granulocyte-monocyte colony stimulating activity (GM-CSA) by isolated human monocytes: response to bacterial endotoxin.

When mononuclear phagocytes are stimulated by bacterial endotoxins, they produce Granulocyte-Monocyte Colony-Stimulating Activity (GM-CSA). In order to study the kinetics of the production of GM-CSA by human monocytes, we prepared suspensions of these cells and studied their response to Salmonella typhi endotoxin. We found that when human monocytes were exposed to this preparation of endotoxin, they synthesized GM-CSA de novo and subsequently secreted it into the extracellular environment; however, within hours, the cells became highly refractory to further stimulation by endotoxin. The resistance to endotoxin which these cells rapidly acquired in vitro could not be accounted for by cell attrition, the accumulation of toxic metabolites in the cultures, negative feedback inhibition by newly synthesized GM-CSA, depolarization of the plasma membrane of the cells, or by degradation of endotoxin. When we studied the binding of tritium-labeled endotoxin to viable monocytes, we found that after monocytes were initially exposed to endotoxin, their subsequent ability to bind lipopolysaccharide molecules onto the surface of the plasma membrane was reduced. When we subjected concentrated supernates from endotoxin-stimulated monocyte cultures to gel filtration and isoelectric focusing, we noted that GM-CSA derived from human monocytes had an apparent molecular weight of approximately 42,000 daltons. Our results indicate that resistance to bacterial endotoxins acquired by mononuclear phagocytes may play a role in the immunologic phenomenon of immediate endotoxin tolerance observed in vivo and may in part be due to down-regulation of endotoxin binding to the outer surface of the cell.

Cells, Cultured↗

Interaction of radiolabeled endotoxin molecules with human monocyte membranes.

Radiolabeled and biologically active endotoxin molecules were prepared, and their binding to monocyte plasma membranes was studied. The binding of 3H-endotoxin and 51Cr-lipid A to isolated membranes was found to be less specific and of lower apparent affinity than that observed using whole cells. Plasma membranes isolated from intact, viable 51Cr-lipid A-pretreated monocytes were found to contain a significant portion of the cell-associated 51Cr-lipid A following Percoll density gradient fractionation of post-nuclear homogenates. When monocytes were pretreated with 3H-endotoxin under the same experimental conditions, all of the label was recovered in the extracellular medium, and subcellular fractionation revealed no fractions which contained tritium. Taken together, our results suggest that specific and high affinity interactions between monocyte membranes and endotoxin molecules are likely to depend on plasma membrane structures which are assembled in intact monocytes but which are disrupted when plasma membranes are isolated from these cells.

Cell Fractionation↗

Heparin affinity: purification of a tumor-derived capillary endothelial cell growth factor.

A tumor-derived growth factor that stimulates the proliferation of capillary endothelial cells has a very strong affinity for heparin. This heparin affinity makes it possible to purify the growth factor to a single-band preparation in a rapid two-step procedure. The purified growth factor is a cationic polypeptide, has a molecular weight of about 18,000, and stimulates capillary endothelial cell proliferation at a concentration of about 1 nanogram per milliliter.

Angiogenesis Inducing Agents↗

Quantitation of serum suppressor factor, related to the erythrocyte receptor of human peripheral blood T lymphocytes as measured by radioimmunoassay.

A solid phase radioimmunoassay for a serum suppressor factor has been developed. The factor was previously purified from malignant ascites fluids and shown to be related to the sheep erythrocyte receptor of human peripheral blood T lymphocytes. This humoral suppressor factor has been termed suppressive E-receptor factor. Using this assay, it was demonstrated that both ascites fluids and sera derived from patients with solid tumors contain elevated levels of this factor compared to similar specimens from patients with a variety of nonmalignant diseases. The concentration of this SER factor does not correlate with serum immunoglobulin G levels but it does correlate with the ability of sera from individual patients to inhibit phytohemagglutinin-induced DNA synthesis by normal human peripheral blood T lymphocytes. Kinetically, this suppressive E-receptor factor directly competes with monoclonal antibody directed to the sheep erythrocyte receptor of human peripheral T lymphocytes and exhibits noncompetitive-type inhibition of DNA synthesis induced by phytohemagglutinin.

Antibodies, Monoclonal↗

Interaction between endotoxin and human monocytes: characteristics of the binding of 3H-labeled lipopolysaccharide and 51Cr-labeled lipid A before and after the induction of endotoxin tolerance.

Salmonella typhi endotoxin (lipopolysaccharide, LPS) was labeled with tritium and purified by gel filtration. Using this preparation, we found that binding of 3H-labeled LPS (3H-LPS) to isolated human monocytes consisted of a rapid (t1/2 less than 5 min), reversible, temperature-independent phase of surface adsorption that was followed by a slower (t1/2 greater than 20 min) period of binding that was irreversible and temperature-dependent. The interactions between 3H-LPS and monocytes that we measured were dependent both on the concentration of LPS and the cell number. We observed an apparent decrease in 3H-LPS surface binding after initial treatment of the cells with LPS, which was most likely due to an acquired reduction in the number of sites on the monocyte membrane available for the binding of LPS. Estimates of the parameters of the binding of 3H-LPS were calculated from a double-reciprocal plot (1/bound vs. 1/free) of the surface binding data and suggest that the relative binding affinity (Kd) for 3H-LPS was unchanged after pretreatment of the monocytes with LPS; however, the total number of LPS binding sites appeared to be reduced by this manipulation. The results of competition binding experiments also suggest that the binding affinity for 3H-LPS was the same before and after incubation of the cells with LPS. Lipid A, which we extracted from LPS and labeled with chromium-51, exhibited a binding affinity similar to that of 3H-LPS and, like 3H-LPS, could be displaced from the cells by competing concentrations of unfractionated LPS; however, the kinetics of binding of the two labeled ligands differed considerably. Our results suggest that exposure of monocytes to LPS may alter the ability of these cells to interact with, and consequently respond to, LPS.

Biological Transport↗

Induction of proliferation of purified human myeloid progenitor cells: a rapid assay for granulocyte colony-stimulating factors.

The proliferation and differentiation of granulocyte and monocyte progenitor cells (CFU-C) in vitro is dependent on the presence of a group of closely related glycoproteins termed colony-stimulating factors (CSF). In order to investigate the interaction of these factors with CFU-C, we purified CFU-C from the peripheral blood of chronic myeloid leukemia patients with an immune rosette technique using specific monoclonal antibodies (mean 74-fold enrichment, 45% cloning efficiency). Colony formation by purified CFU-C demonstrated an absolute dependence on an exogenous source of CSF. Liquid culture of small aliquots of enriched CFU-C with CSF-containing medium resulted in a rapid, time- and concentration-dependent induction of DNA synthesis as measured by 3H-thymidine incorporation. This specific CSF induction of DNA synthesis by enriched CFU-C was used to develop a microassay system for CSF activity. CSF activity could be reproducibly quantitated in 24-48 hr. The proliferating cells in this assay system were shown to be myeloid progenitor cells by examining the morphology of their progeny and by determining the surface antigen phenotype of the responding cells (Ia+, T3-, B1-, Mo1-). This microassay provides a quantitative assessment of CSF activity that may be useful in the purification of human CSF and in the generation of monoclonal antibodies to CFU-C surface structures.

Animals↗

The production of granulocyte-monocyte colony-stimulating activity by isolated human T lymphocyte subpopulations.

Isolated human T lymphocyte subpopulations were obtained by fluorescence-activated cell sorting using the murine monoclonal antibodies, OKT4 and OKT8. The capabilities of the isolated lymphocytes to produce granulocyte-monocyte colony-stimulating activity (CSA) in response to mitogen challenge were assessed by in vitro assays employing light density nonadherent bone marrow cells. Essentially, no CSA production was noted by any isolated T lymphocyte population [OKT4 positive (+) or OKT8 positive (+)] cultured alone or following the addition of 10(4) autologous monocytes/ml. When phytohemagglutinin (PHA) alone was added, OKT4+ lymphocytes elaborated small amounts of CSA. With the addition of concanavalin A (Con-A) alone, both OKT4+ and OKT8+ cells were able to produce modest amounts of CSA. Significantly enhanced CSA production was observed when either OKT4+ or OKT8+ lymphocytes were coincubated with autologous monocytes in the presence of mitogen. We conclude that highly purified T lymphocyte subpopulations, free of monocytes as assessed by nonspecific esterase staining, can elaborate small amounts of CSA in response to PHA or Con-A challenge. A synergistic augmentation of CSA production was noted with coincubation of sorted lymphocytes and autologous monocytes in the presence of mitogen. Finally, our results suggest that the ability of T lymphocytes to make CSA is not exclusively limited to either the OKT4+ or OKT8+ defined subsets.

Antibodies, Monoclonal↗

The effects of tumor-promoting phorbol esters on human granulopoiesis in vitro.

In order to determine whether the tumor-promoting phorbol esters are capable of inducing normal human committed granulocytic-monocytic progenitor cells (CFUc) to proliferate and differentiate in the absence of granulocyte-monocyte colony-stimulating activity (CSA), we studied the effects of these compounds on human granulopoiesis in vitro. We found that when light-density human marrow cells or peripheral blood leukocytes were depleted of adherent cells and then incubated in semisolid tissue culture medium under conditions optimal for CFUc growth, phorbol myristate acetate (PMA) and its congeners produced no measurable stimulatory effect on the proliferation of CFUc in the absence of added CSA. Likewise, when light-density marrow cells that had not been depleted of adherent cells were plated in the cultures, no stimulation of CFUc colony growth resulted from the addition of PMA. However, when light-density peripheral blood leukocytes were used as a target source of CFUc without first subjecting them to adherence separation, enhanced proliferation and differentiation of CFUc were noted in cultures that contained PMA. To investigate the possibility that CSA production by monocytes in these cultures in response to activation by PMA might account for the enhanced colony formation that we observed, we incubated isolated peripheral blood monocytes in short-term liquid suspension cultures and found that in the presence of PMA, large quantities of CSA were secreted into the surrounding medium. Finally, we noted that when marrow cell suspensions were suboptimally stimulated by low concentrations of CSA added to the cultures, the effects of PMA on CFUc proliferation were unpredictable, enhancing colony formation in some cases and inhibiting it in others. Our data indicate that although the tumor-promoting phorbol esters do not appear capable of directly stimulating the proliferation or differentiation of human CFUc in the absence of CSA, they may do so indirectly by causing auxiliary cells such as monocytes to secrete CSA.

Bone Marrow↗

Acute chemical meningitis after metrizamide-lumbar myelography.

Severe acute meningitis developed after the use of metrizamide for lumbar myelography; cerebrospinal fluid findings included a white blood cell count of 2300, mostly polymorphonuclear cells, glucose level of 8 mg% and protein level of 253%. This apparent chemical meningitis could not be distinguished, either clinically or by cerebrospinal fluid examination, from acute bacterial meningitis. This case emphasizes that severe acute meningeal reactions, while very rare, can occur after the use of metrizamide for myelography. Such patients must be evaluated promptly to rule out bacterial meningitis and should be followed carefully for possible later sequelae.

Acute Disease↗

The synthesis and secretion of granulocyte-monocyte colony-stimulating activity (CSA) by isolated human monocytes: kinetics of the response to bacterial endotoxin.

We studied the kinetics of the synthesis and secretion of granulocyte-monocyte colony-stimulating activity (CSA) by human monocytes stimulated by S. typhi endotoxin. We found that these cells initially secrete copious quantities of CSA when exposed to endotoxin but rapidly become refractory to its stimulatory effect. When monocytes were incubated in liquid suspension cultures, large amounts of CSA were generated during the first 24 hr of culture after the addition of as little as 10 ng/ml of endotoxin to previously unstimulated monocytes. After the addition of endotoxin, CSA secretion abruptly took place after an initial 1 to 2 hr lag phase, and occurred primarily within the first 6 to 12 hr of culture. The addition of puromycin or cycloheximide to the cultures significantly inhibited CSA secretion in response to endotoxin, suggesting that CSA production by stimulated monocytes requires de novo protein synthesis and does not solely result from the release of preformed active CSA. After initial exposure to endotoxin, CSA production by monocytes steadily decreased after 24 hr and ceased after 72 hr. Subsequent reexposure to the same concentration of endotoxin resulted in little CSA production, whereas the refractory state could be overcome by increasing the quantity of endotoxin added. Additional studies demonstrated that refractoriness of monocytes to further CSA production after initial response to endotoxin was not due to a loss of cell viability, degradation of endotoxin, or inhibition of CSA synthesis by soluble metabolites generated by stimulated monocytes. Our data suggest that the capacity of human monocytes to synthesize CSA in response to endotoxin rapidly becomes blunted after initial exposure of the cells to the lipopolysaccharide, but that the refractory state of these cells can be overcome by increasing the concentration of endotoxin. Acquired hyporesponsiveness of cells that produce CSA may in part account for the phenomenon of immediate endotoxin tolerance observed in vivo.

Cell Separation↗

Stimulation of increased capillary endothelial cell motility by chondrosarcoma cell-derived factors.

The ability of chondrosarcoma cell-derived preparations to stimulate an increase in the motility of bovine capillary endothelial (BCE) cells was quantitated using a phagokinetic track assay which measures the area of tracks produced by BCE cells after ingestion of gold particles. Chondrosarcoma preparations stimulated a 2-fold increase in the mean track area produced by BCE cells in an 18-hr incubation period. The motility-stimulating activity of chondrosarcoma was purified about 120-fold. The most highly purified fractions had molecular weights between 16,000 and 20,000 and stimulated a 2-fold increase in BCE cell motility at concentrations of 10 to 20 ng/ml.

Animals↗

The role of intraoral and gastrointestinal cues in the control of sucking and milk consumption in rat pups.

Nutritive deprivation, suckling deprivation, gastronintestinal fill, and milk availability contribute to the control of sucking (as measured by jaw-muscle electromyograph) and ingestion of milk (provided via a tongue cannula) in 11-13-day-old rat pups. Depriving pups of the opportunity to suckle reliably increases subsequent sucking and milk intake. Intraoral delivery of milk also increases sucking, regardless of whether or not pups are suckling-deprived. Gastrointestinal preloads have no effect on sucking if pups are not receiving milk, but reliably block the increase in sucking which accompanies milk delivery. Finally, milk delivered to the pup's mouth prior to a suckling opportunity can either enhance or attenuate subsequent sucking depending on whether pups are allowed to consume milk while suckling. In all cases, a particular mode of sucking ("rhythmic" sucking) is most affected by experimental manipulation, and appears to be an important component of the pup's ingestive behavior.

Animals↗

Short- and long-term effects of various milk-delivery contingencies on sucking and nipple attachment in rat pups.

Varied milk delivery contingencies differentially affect sucking in rat pups as measured by jaw-muscle electromyographic activity. In Experiment I we found that 11-13-day-old pups sucked more frequently when receiving tiny intermittent pulses of milk than when receiving no milk, and continued to suck at a high rate for at least 30 min after cessation of milk delivery. In subsequent experiments we found that pups 13-18 days of age engaged in more frequent sucking if receiving milk continuously rather than intermittently, and that this increased rate of sucking persisted for at least 24 hr after cessation of milk delivery. Pups given experience with continuous milk delivery from 14 to 18 days of age also spent significantly more time attached to the nipple at 19 days of age than did pups in control groups. It was concluded that experience with different milk delivery schedules can affect subsequent sucking and nipple attachment behavior.

Animals↗

The role of colony stimulating activity in modulating murine diffusion chamber granulopoiesis.

We studied the effects of high circulating Colony Stimulating Activity (CSA) levels and irradiation induced marrow hypoplasia in CF1 and C57B1/6J host mice upon granulopoiesis in intraperitoneal diffusion chamber (DC) cultures. Serial endotoxin injections resulted in marked elevation of circulating CSA for the first half of an 8 d culture period, and CSA was shown to diffuse into the chamber environment; yet this manipulation alone did not significantly accelerate DC cell growth. Pre-irradiation of the host mice produced no elevation of circulating CSA during the early phase of culture, but resulted in significant stimulation of DC granolopoiesis. Fluctuations in circulating inhibitors of in vitro granulopoiesis did not correlate well with DC cellularity. We conclude that endogenous CSA elevation does not providean effective stimulus per se for granulocyte-monocyte proliferation within DC culture and cannot be solely responsible for mediating the exuberant DC granulopoietic response seen in the pre-irradiated host.

Animals↗