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Biomedical subjects

R Urbaschek

Publications and source records attributed to R Urbaschek.

47 records · Page 3Linked to original sources
PubMed1979

Effects of bacterial products on granulopoiesis.

Methylated endotoxin and Freeman-type polysaccharide each stimulate granulopoiesis and the production of CSF in mice. These same preparations also protect pretreated mice from lethal X-irradiation. The role of CSF in stimulating granulopoiesis in vivo was shown by the ability of anti-CSF to reduce the number of CFUc in endotoxin-treated mice. C3H/HeJ low responder mice cannot be protected against lethal X-irradiation by pretreatment with endotoxin and they fail to produce CSF in response to phenol water extracted endotoxin and the Freeman-type polysaccharide, but do respond to trichloroacetic acid endotoxin with elevated serum CF levels.

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PubMed1979

Prostaglandin regulation of colony-stimulating factor production by lipopolysaccharide-stimulated murine leukocytes.

The production of colony-stimulating factor by lipopolysaccharide-stimulated murine peritoneal leukocytes and their adherent subpopulations (greater than 80% macrophages) was markedly enhanced by indomethacin at concentrations sufficient to block prostaglandin E synthesis. Addition of physiological concentrations of E-series prostaglandins reversed this enhancing effect of indomethacin in a dose-dependent manner. These results indicate that colony-stimulating factor production by stimulated leukocytes is regulated by E-series prostaglandins and suggest that prostaglandins function to limit myelopoiesis by inhibiting colony-stimulating factor production and concomitantly the induction of cell proliferation.

Animals↗
PubMed1979

The inflammatory response to endotoxins.

1. Endotoxins are very potent and widely spread inflammation-inducing substances. 2. In the course of local infections endotoxins represent one of the main principles of the pathogenicity of gram-negative bacteria by inducing acute nonspecific inflammation. 3. The pharmacological activities of endotoxins consist primarily in generating and liberating the classic mediators of acute nonspecific inflammation. 4. Endotoxins are able to enter into the circulation through their capicity to activate pharmacological mediators. 5. The endotoxic mediators which increase the permeability of the microcirculation of the intestinum enable endotoxins as components of the physiological intestinal flora to enter into the circulation; these induce systemic disease or shock depending on their concentration in the circulation. 6. In the course of chronic inflammation recidivism or recrudescence as trasient acute inflammatory outburst can be caused by local effects of endotoxins. 7. According to some recent observations the inflammation inducing capacity of endotoxins may promote the entry of aerobic bacteria into the blood stream which can result in mixed septicemia.

Animals↗
PubMedDate not supplied

Tumor necrosis factor and interleukin 1 as mediators of endotoxin-induced beneficial effects.

Bacterial lipopolysaccharides or endotoxins are known to induce tumor necrosis; enhanced nonspecific resistance to bacterial, viral, and parasitic infections and to radiation sickness; and tolerance to lethal doses of endotoxin. These beneficial effects are achieved by pretreatment with minute amounts of endotoxin. Recombinant tumor necrosis factor (TNF) and interleukin 1 (IL-1) are among the mediators capable of invoking radioprotection or resistance to the consequences of cecal ligation and puncture. Both cytokines are potent inducers of serum colony-stimulating factor (CSF) in C3H/HeJ mice (low responders to endotoxin). The number of splenic granulocyte-macrophage precursors was found to increase 5 days after injection of TNF in these mice. Although with IL-1 no increase in the number of granulocyte-macrophage colonies occurred in culture in the presence of serum CSF, a marked stimulation was observed when TNF was added. This stimulation of myelopoiesis observed in vivo and in vitro may be related to the radioprotective effect of TNF. The data presented suggest that TNF and IL-1 released after injection of endotoxin participate in the mediation of endotoxin-induced enhancement of nonspecific resistance and stimulation of hematopoiesis.

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PubMedDate not supplied

Kupffer cell function in host defense.

High-resolution in vivo microscopic methods have been used to explore the responses to endotoxin of Kupffer cells in the livers of anesthetized mice, rats, hamsters, and guinea pigs under a variety of experimental conditions. These include studies of normal animals as well as of animals sensitized or tolerant to endotoxin, C3H/HeJ mice with a low response to endotoxin, mice rendered septic by cecal ligation and puncture, mice with Kupffer cells selectively destroyed by frog virus 3, and rats with portacaval shunts. The functional state of Kupffer cells was evaluated by measuring both the number of these cells per microscopic field that phagocytosed 1.0-micron latex particles and the rate at which individual Kupffer cells phagocytosed single latex particles. The intrahepatic density and level of activation of Kupffer cells were found to play a role in determining endotoxin sensitivity and to be involved, in conjunction with endotoxin, in the development of tolerance. All of these studies support the concept of a central role for Kupffer cells in host defense mechanisms and of the possible modulation and of this role by gut-derived endotoxins contained in the portal blood.

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