Effects Of Bacterial Endotoxin Research Articles

Effect of bacterial endotoxin on the course of Plasmodium berghei infection

The intraperitoneal administration of certain doses of bacterial ( Escherichia coli) endotoxin to mice has been shown to significantly suppress Plasmodium berghei parasitemia levels and to extend survival of the host. Single doses of 20 μg endotoxin given the day before the injection of 10 7 parasitized RBC extended the usual one-week survival period by about one day. Each daily count of parasitized RBC from mice treated with endotoxin was comparable to the previous day's count for the saline-treated controls. Of the various doses tested, the best results from single injections were obtained with the 20-μg doses. Repeated injections of endotoxin were only slightly more effective than single injections. The similar influence of endotoxin on the course of intravenously induced P. berghei infections demonstrated that the action of endotoxin is not simply a matter of inhibition of passage of malarial inoculum from the peritoneal cavity into the bloodstream. The suppressive influence of endotoxin on P. berghei infections could also be produced in rats. This inhibitive effect of endotoxin may be related to nonspecific stimulation of factors of resistance.

Endotoxin-enhanced Host Resistance: Reversal by Kinetin Riboside

KINETIN riboside (6-furfurylaminopurine riboside) reverses the stimulatory effects of oligodeoxyribonucleotides on antibody synthesis1 and phagocytosis2. Evidence exists suggesting that some of the effects of bacterial endotoxins on increased host-resistance to pathogens may be associated with a release of such oligomers3, and it was considered of interest to determine the influence of kinetin riboside on the protective effects of endotoxin.

Effects of Bacterial Endotoxin on the Occurrence of Spleen Colonies in Irradiated Mice

It is generally agreed that survival in the midlethal radiation dose range depends principally on hemopoietic recovery. Administration of endotoxin as a single injection either before or shortly after irradiation in the mouse hastens recovery of granulocytes, erythrocytes, platelets, and lymphocytes (1, 2), increases resistance to infection (3), and reduces mortality (4). In contrast, multiple injections given before irradiation cause no advance in leukocyte recovery or increase in survival (4, 5), even though such injections in nonirradiated mice cause greater increases in spleen weight and resistance to bacterial challenge than a single injection. Till and McCulloch have observed that nodules seen in the spleen 10 days after irradiation are erythroid, granulocytic, megakaryocytic, or mixed (6) and that their number is related to radiation dose and survival (7, 8). The present experiments show that a single injection of endotoxin increases splenic nodules as well as granulocyte count and survival. In contrast, the multiple injections increase the number of splenic nodules (though to a lesser extent) without promoting marrow recovery or survival.

The protective effect of endotoxin in x-irradiated mice.

In mice X-irradiated with lethal dose (750 r) and mid-lethal dose (550 r) the protective effect of bacterial endotoxin isolated from strains ofSalmonella typhi has been found to be limited to a short period before irradiation and administration of endotoxin in repeated doses did not enhance protection. Application of endotoxin 4 days after X-rays resulted in increase of lethality of irradiation and earlier deaths of experimental animals were observed. Active intravenous and intraperitoneal immunization with endogenous strains ofEscherichia coli isolated from the intestinal flora of mice had a demonstrable protective effect when compared with passive immunization.

Chemical Analyses of the Blood of Chicks Infected or Endointoxicated with Escherichia coli

INTRODUCTIONTHE effect of bacterial infections on blood constituents has been investigated. Dooley, Holtman and Jeffries (1958) reported that the blood glucose level decreased when chicks were infected with Salmonella pullorum. Ross et al. (1956) and Dooley et al. (1958) observed that the blood creatinine and blood urea nitrogen (BUN) levels increased when chicks were infected with this organism.The effect of bacterial endotoxins has also been investigated in numerous animal species. Dooley et al. (1958) have found that the concentrations of some components were altered during intoxication by S. pullorum endotoxin. However, avian species do not normally suffer lethal effects from injections of bacterial endotoxins (Ball et al., 1962).Normal values of blood constituents have been recorded by Groebbels (1932), Dyer and Roe (1934), Henry et al. (1934), and Sturkie (1954). Due to differences in breed, age, diet, number of samples, and procedures employed, the data in the literature…

Effects of Bacterial Endotoxin on Metabolism: Role of Tryptophan Pyrrolase in Response of Mice to Endotoxin

Effects of Bacterial Endotoxin on Metabolism: Role of Tryptophan Pyrrolase in Response of Mice to Endotoxin

EFFECT OF BACTERIAL ENDOTOXIN ON THE PHAGOCYTIC ACTIVITY OF THE RETICULO-ENDOTHELIAL SYSTEM IN RABBITS OF DIFFERENT AGE.

Stimulation of the phagocytic activity of the reticulo-endothelial system with bacterial endotoxin was studied in newborn rabbits in the period in which they do not actively form antibodies to bacterial antigens. A markedly accelerated clearance of colloidal carbon from the blood was found in five-day-old rabbits (tested by the technique of Biozzi, Benacerraf and Halpern 1953) when relatively high doses of endotoxin were used. It is assumed that the increased resistance to infection which may be elicited in young animals in that period is due to stimulation of cellular defence mechanisms. By comparison of the stimulating effect of endotoxin on phagocytosis in five-day-old, one-month-old and adult rabbits it was found that the phagocytic cells of the R.E.S. are more susceptible to the effect of endotoxin in adults than in newborns. This difference is evident from comparisons of the phagocytic indices K and the corrected phagocytic indices α in three age groups of rabbits stimulated with different doses of endotoxin. The possible mechanism and cause of differences in sensitivity of young and adult individuals is discussed.

Effect of Bacterial Endotoxin on Leucocytes of Tuberculin Sensitive Hosts

Effect of Bacterial Endotoxin on Leucocytes of Tuberculin Sensitive Hosts

Production of fever in rabbits with extracts of tissue culture cells infected with Coxsackie virus.

Abstract The following experiments describe the characteristics of the fever produced in rabbits by Coxsackie virus grown in monkey kidney cells. Viruses grown in tissue culture have not previously been shown to produce fever. The tissue culture system affords the advantage of excluding the possibility of contamination by leukocytic pyrogen which could conceivably occur in the chick embryo. Monkey kidney cells, either whole or disrupted, which had not been inoculated with virus failed to produce fever following injection into rabbits. Consistent fevers were produced, however, by aliquots of disrupted cells containing Coxsackie B-1 virus. The fever regularly followed a latent period of 45 minutes and produced 2 peaks, one at 90 minutes and one at 3 to 4 hours. Identical fevers were produced in rabbits previously made tolerant to the fever-producing effect of bacterial endotoxin. Rabbits injected on consecutive days with Coxsackie virus pyrogen exhibited tolerance by the third day. The pyrogenic activity was not diminished even though aliquots were heated to 70 °C. for 30 minutes, indicating that the fever is not due to active infection. These findings indicate that extracts of monkey kidney cells infected with Coxsackie virus in the absence of leukocytes produce a characteristic fever following intravenous injection into rabbits. Attempts to obtain similar results with adenovirus and vaccinia virus grown in HeLa cells were not successful.

Effect of bacterial endotoxin in germ-free mice.

SummaryGerm-free and conventionally reared mice of similar genetic stock maintained on the same sterilized diet were compared as to their reaction to bacterial endotoxin. No significant difference was found in the following: elevation in levels of antibody to Gram-negative bacteria, stimulation of glycolytic activity of spleen cells and peritoneal macrophages, susceptibility to infection with Salmonella typhosa, production by endotoxin of increased resistance to infection, and LD50 of endotoxin.

The effect of bacterial endotoxin on repair in connective tissue

Summary o 1. Under the conditions of these experiments, there is no evidence that the administration of a bacterial endotoxin favorably affects normal repair by connective tissue as measured by the formation of collagen, gain in tensile strength or rate of contraction. In fact, in repeated doses it may inhibit repair. 2. A suboptimal rate of growth as observed around implanted plastic sponges is stimulated by the administration of endotoxins in appropriate doses. 3. This study provides additional evidence that there is a specific relation between the initial inflammatory response to injury and the rate of connective tissue formation. There appears to be an optimal inflammatory response beyond which stimulation is deleterious.

Sensitivity of mice to bacterial lipopolysaccharide following alteration of activity of the reticulo-endothelial system.

It has generally been assumed that resistance of animals to the pyrogenic and lethal effects of bacterial endotoxin is largely dependent on the phagocytic capacity of the reticulo-endothelial system. Thus it has been shown that stimulation of the reticulo-endothelial system with non-lethal doses of bacterial lipopolysaccharide or endotoxin results in protection of the animals against a subsequent lethal dose of endotoxin1. Again, numerous workers have demonstrated that a ‘blockade’ of the reticulo-endothelial system by colloidal particles, for example saccharated iron oxide, thorotrast and trypan blue, increases the sensitivity of the animals to the lethal effects of these substances2. Recently, however, it has been shown that in certain circumstances it is possible for mice to possess an increased phagocytic activity, as measured by their ability to clear colloidal carbon, and yet be highly sensitive to the effects of endotoxin. This can be seen during the course of an intracellular infection3, or following the administration of zymosan4. The apparent contradiction of these results has yet to be resolved, and it is not unlikely that such resolution may lead to an elucidation of the mode of action of the endotoxins.

Modification of lethal effect of bacterial endotoxin by substances altering the metabolism of 5-hydroxytryptamine.

SummaryThe lethal effect of bacterial endotoxin in mice is modified by administration of the 5HT antagonist, BAS, the monoamine oxidase inhibitor PIH, or the 5HT precursor, 5 HTP. Animals pretreated with BAS and 5 HTP demonstrated increased resistance to endotoxin whereas pretreatment with PIH increased susceptibility to endotoxin.

Adrenergic inhibition and lethal effect of bacterial endotoxin in mice.

Summary1) Protective effects of various types of adrenergic inhibition have been tested against lethal action of injected bacterial endotoxin in mice. 2) Preliminary experiments substantiated abilities of phenoxybenzamine to block lethal effect of injected epinephrine and of cocaine to augment its toxicity. 3,4-Dichloroisoproterenol also increased lethal effect of epinephrine. TM 10, or 2,6-xylyloxyethyltrimethylammonium bromide had no effect acutely but offered low order of protection when given 24 hours before epinephrine. Reserpine also protected when given 24 hours in advance. Iproniazid was without effect. 3) Against bacterial endotoxin from E. coli the only compound to give significant protection was 3,4-dichloroisopreterenol. This substance has been shown by previous workers to block inhibitor and vasodilator effects of epinephrine and related catechol amines. Such effects are probably metabolic in nature and may concern carbohydrate metabolism.

Effect of Bacterial Endotoxin on Resistance of Mice to Viral Encephalitides

Summary Purified endotoxin prepared from Salmonella abortus equi enhanced the resistance of mice to infection with the viruses of eastern equine encephalomyelitis (EEE) and encephalomyocarditis (EMC). The protective effects were manifested by a moderate reduction in incidence of death and slight, but definite, prolongation of survival time. Increased resistance could be demonstrated in infections initiated by either the intracerebral or intraperitoneal route. A single dose of endotoxin administered i.p., i.v. or i.c. 24 hours before challenge was often effective. However, combined i.p. and i.c. injections of endotoxin further augmented resistance to i.p. infection with EEE or EMC virus, and the most pronounced effect was evident in mice given repeated i.p. doses of endotoxin. In contrast to previous studies of “nonspecific” resistance to bacterial infection or viral toxicity, a favorable outcome was also demonstrable when endotoxin was administered concomitantly with challenge virus or when a course of treatment was begun 6 hr after i.p. infection with EEE virus. Endotoxin-induced resistance to the lethal action of EEE virus was accompanied by moderate inhibition of virus multiplication in brain. Endotoxin had no effect on multiplication of EEE virus in tissue culture, nor could it be shown to stimulate the production of an antiviral substance in brain. Certain differences were noted between endotoxin-induced resistance to viral encephalitis and the viral interference phenomenon. Intracerebral injection of influenza virus caused striking resistance to infection with EEE virus and marked inhibition of virus multiplication in brain. Although the capacity of influenza virus to protect mice against infection with EMC virus was slightly greater than that of bacterial endotoxin, no effect could be demonstrated unless the interfering virus was injected directly into the brain. Unlike bacterial endotoxin, influenza virus effectively suppressed multiplication of EEE virus in tissue cultures of chicken embryo fibroblasts.

Effect of Bacterial Endotoxins on Platelets and Release of Serotonin (5-Hydroxytryptamine) I

Effect of Bacterial Endotoxins on Platelets and Release of Serotonin (5-Hydroxytryptamine) I

Effect of Bacterial Endotoxins on Platelets and Release of Serotonin (5-Hydroxytryptamine) II

Effect of Bacterial Endotoxins on Platelets and Release of Serotonin (5-Hydroxytryptamine) II

Effect of Bacterial Endotoxins on Glycogen Synthesis.

SummaryIntraperitoneal injection of Salmonella endotoxin completely inhibited in vivo glycogen synthesis from glucose in the liver of rats. In liver slices of rabbits, there was less glycogen formed in vitro from glucose and pyruvate in the presence of meningococcal endotoxin. The glucose uptake of rat diaphragm in vitro was decreased by Salmonella endotoxin and this inhibition of glucose utilization could be diminished by the addition of insulin.

Effect of Bacterial Endotoxins on Carbohydrate Metabolism of Rabbits.

Effect of Bacterial Endotoxins on Carbohydrate Metabolism of Rabbits.