The Role of Colony Stimulating Activity in Modulating Murine Diffusion Chamber Granulopoiesis

Sullivan, Richard; Zuckerman, Kenneth S.; Quesenberry, Peter J.

doi:10.1111/j.1365-2141.1980.tb05905.x

Cited by 9 publications

(2 citation statements)

References 14 publications

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“…Intraperitoneal implantation of diffusion chambers (DC) in live murine hosts has provided a useful model for the study of in vivo regulation of granulopoiesis (Benestad, 1970;Quesenberry et al, 1974). Utilizing this technique, two groups of investigators (Rothstein et al, 1971(Rothstein et al, , 1973Sullivan et al, 1980) have shown that alterations in CSA do not adequately explain the fluctuations that occur in DC granulopoiesis after a variety of experimental manipulations. Rothstein et al (1971Rothstein et al ( , 1973 have described a humoral regulator of granulopoiesis in DC, termed diffusible granulocytopoietic stimulator (DGS), which is experimentally distinct from both CSA and neutrophil-releasing factor.…”

Section: Discussionmentioning

confidence: 99%

Further studies on the mechanism of marrow granulocytic hyperplasia in mice chronically injected with endotoxin

Levitt

Quesenberry

1982

Br J Haematol

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Marrow granulocytic hyperplasia occurs regularly in mice injected with endotoxin for 7--30 d, despite minimal elevations of serum colony-stimulating activity (CSA). Alterations in marrow granulocyte-monocyte progenitor (CFU-C) number of changes in marrow cell cycle status do not explain this hyperplasia. We have studied other mechanisms which may explain this increased granulopoiesis. CF1, BDF1 or C57bl/6J mice were infected with 10 micrograms of S. typhosa endotoxin i.p. daily for 7--20 d. Control and endotoxin injected (tolerant) sera, each with identical levels of CSA, were assayed against control marrow cells stimulated with supramaximal amounts to CSA to assess the role of serum potentiators in augmenting granulopoiesis. In six separate experiments, tolerant sera, over a 30-fold concentration range, produced a 1.7--4.0-fold potentiation of colony growth compared to control sera (P less than 0.001). No increased tolerant sera potentiation was seen over a similar concentration range when assayed against tolerant marrow. Tolerant and control splenic conditioned media, both dialysed and non-dialysed, failed to potentiate control marrow colony growth. Tolerant marrow stem cells did not show changes in CSA sensitivity, colony size distribution or differentiation, and tolerant bone or bone marrow cells did not produce increased amounts of CSA. We conclude that serum factors separate from CSA may in part explain the increased granulopoiesis seen in endotoxin injected mice. The failure of tolerant sera to potentiate tolerant marrow growth in vitro may reflect prior in vivo exposure of marrow to these potentiating factor(s).

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Section: Discussionmentioning

confidence: 99%

Further studies on the mechanism of marrow granulocytic hyperplasia in mice chronically injected with endotoxin

Levitt

Quesenberry

1982

Br J Haematol

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“…1). 3H-LPS prepared in this manner retained potent endotoxic bioactivity as assessed by its ability to coagulate limulus lysate (Mallinckrodt Laboratories, St. Louis, MO), to elevate the plasma concentration of GM-CSF within 4 hr after injection into CF1 mice (30), and to stimulate isolated human monocytes to secrete GM-CSF activity when added to liquid suspension cultures of these cells at 0.5-1.0 lg/ml (18). For these biologic assays, murine (30) and human (31) GM-CSF was quantified by using tissue culture bioassays that we have described previously.…”

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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.

Larsen¹,

Sullivan²

1984

Proc. Natl. Acad. Sci. U.S.A.

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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 (t½2 < 5 min), reversible, temperature-independent phase of surface adsorption that was followed by a slower (t,,2 > 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.Bacterial lipopolysaccharides (LPSs), or endotoxins, are macromolecular complexes that produce an extraordinary array of pathophysiologic effects in susceptible cells (1). A number of types of mammalian cells respond to stimulation by endotoxin (2-4); however, it is clear that a primary target cell for its action is the mononuclear phagocyte. Very low concentrations of endotoxin greatly increase the phagocytic (5, 6) and pinocytic (5, 7) function of monocytes and macrophages, induce tumor cytotoxicity mediated by these cells (8-10), activate synthesis and release of their lysosomal enzymes (6,11,12), increase the proliferation of mononuclear phagocytes (13-15), and greatly enhance the production of granulocyte-monocyte colony stimulating factors (GM-CSF) by these cells (16)(17)(18).The development of tolerance to the stimulatory and toxic effects of endotoxin is a well-recognized yet poorly understood phenomenon (19). Of major interest to our laboratory has been the resistance to the GM-CSF-elevating effects of endotoxin, which occurs within hours in experimental animals after their initial injections with bacterial LPSs (20,21 Relatively little is known about the molecular mechanisms that control the initial response of cells to endotoxin and the subsequent development...

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The in vivo diffusion chamber technique for bone marrow or blood cell culture

Willemze

Walker

1981

Blut

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The Role of Colony Stimulating Activity in Modulating Murine Diffusion Chamber Granulopoiesis

Cited by 9 publications

References 14 publications

Further studies on the mechanism of marrow granulocytic hyperplasia in mice chronically injected with endotoxin

Further studies on the mechanism of marrow granulocytic hyperplasia in mice chronically injected with endotoxin

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.

The in vivo diffusion chamber technique for bone marrow or blood cell culture

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