scholarly journals EFFECTS OF BACTERIAL ENDOTOXINS ON METABOLISM

1961 ◽  
Vol 113 (1) ◽  
pp. 83-94 ◽  
Author(s):  
L. Joe Berry ◽  
Dorothy S. Smythe
Keyword(s):  
Iron Oxide ◽  
Subcutaneous Administration ◽  
Reticuloendothelial System ◽  
Normal Serum ◽  
Nitrogen Excretion ◽  
Mouse Serum ◽  
E Coli ◽  
Bacterial Endotoxins ◽  
Urinary Nitrogen

There exists an inverse proportionality between number of heat-killed cells of Salmonella typhimurium injected intraperitoneally into mice and the quantity of urinary nitrogen the animals excrete during a 17 hour period following the subcutaneous administration of 2 units of ACTH. This relationship has been developed into an assay for bacterial endotoxin. Mice immunized against S. typhimurium require 10 to 20 times the number of cells needed by control animals to suppress urinary nitrogen excretion to the same extent. Intravenous saccharated iron oxide sensitizes animals so that fewer heat-killed salmonellae can be detected. Heat-killed cells of Staphylococcus aureus are without effect in the assay. Several lipopolysaccharides derived from Gram-negative bacteria are effective in preventing the rise of urinary nitrogen excreted in response to ACTH and the amount required, compared to the LD50, is in the same ratio for all of them. Citrated mouse serum partially inactivates the endotoxin during in vitro incubation for 1 hour at 37°C. while normal serum does not. Dichloroisoproterenol protects mice against the lethal effects of lipopolysaccharide and it lowers its effectiveness in the assay. The minimum amount of endotoxin reliably determined by the test is 0.25 µg. of an E. coli preparation that was given intravenously in mice in which the reticuloendothelial system had been "blocked" with saccharated iron oxide.

scholarly journals EFFECTS OF BACTERIAL ENDOTOXINS ON METABOLISM

1962 ◽  
Vol 116 (6) ◽  
pp. 897-911 ◽  
Author(s):  
L. Joe Berry ◽  
Dorothy S. Smythe ◽  
Susannah McC. Kolbye
Keyword(s):  
Nitrogen Excretion ◽  
Protein Nitrogen ◽  
Bacterial Endotoxins ◽  
Small Change ◽  
The Moment ◽  
Lower Ratio ◽  
Urinary Nitrogen Excretion ◽  
Urinary Nitrogen

The greater susceptibility to the lethal effects of bacterial endotoxin (heat-killed Salmonella typhimurium or Escherichia coli lipopolysaccharide, in mice infected with an attenuated strain of Mycobacterium tuberculosis (BCG) was confirmed. It reached a maximum at 2 weeks postinfection and gradually diminished for an additional 6 weeks. At the time of maximum susceptibility several metabolic and physiological differences became apparent. BCG-infected mice die sooner (4 to 12 hours) and without the diarrhea, conjunctivitis, and general symptomatology associated with endotoxin deaths of normal animals. Reticuloendothelial blockade results in only a small change in reactivity to endotoxin, in contrast to normal mice. Subcutaneous injection of 2 units of ACTH is followed by no significant increase in urinary nitrogen excretion while in control animals it more than doubles. Plasma clearance of intravenously administered inulin is approximately normal in BCG-infected mice 17 hours after an LD50 dose of endotoxin but control mice similarly treated show renal impairment. In line with this result is the absence of elevated carcass non-protein nitrogen (NPN) following endotoxin poisoning or at the moment of death from endotoxemia in the hyperreactive animals in contrast to the two- to threefold increase in carcass NPN in normal mice under similar conditions. Body carbohydrate is at a minimum and becomes depleted to a level approximating that found at death more rapidly in BCG-infected mice given endotoxin than in controls. There is also a lower ratio of carbohydrate anabolized to protein catabolized following cortisone administration to BCG-infected mice than in control mice. This is found in adrenalectomized mice and in stressed animals and is reported elsewhere. Some of the differences just described can be attributed to a refractory adrenal cortex. There is less depletion of adrenal cholesterol in vivo and lower corticoid synthesis in vitro than in normal mice yet this is not fundamentally responsible for the greater susceptibility of BCG-infected animals to endotoxin since adrenalectomized mice, which are even more susceptible, are metabolically and physiologically more comparable to normal mice than to BCG-infected mice. One can conclude, therefore, that the hyperreactivity of BCG-infected mice is more than an intensification of the normal response to endotoxin.

scholarly journals Effects of ractopamine hydrochloride on nutrient digestibility and nitrogen excretion of finishing beef cattle

2021 ◽  
Author(s):  
B N Harsh ◽  
B J Klatt ◽  
M J Volk ◽  
A R Green-Miller ◽  
J C McCann
Keyword(s):  
Rumen Fluid ◽  
Block Design ◽  
Dietary Treatment ◽  
Feedlot Cattle ◽  
Nutrient Digestibility ◽  
Nitrogen Excretion ◽  
Distillers Grains With Solubles ◽  
Ractopamine Hydrochloride ◽  
Urinary Nitrogen

Abstract The objective was to quantify the effects of the beta-adrenergic agonist (β-AA) ractopamine hydrochloride (Actogain, Zoetis, Parsippany, NJ) on nitrogen excretion and nutrient digestibility in feedlot cattle. In experiment 1, twelve Simmental × Angus steers were blocked by bodyweight (531 ± 16 kg) and used in a randomized complete block design. Dietary treatments included: 1) a control without β-AA (CON) or 2) 400 mg/steer/d ractopamine hydrochloride (RAC) for 35 d before slaughter. Diets contained (DM basis) 55% dry rolled corn, 20% corn silage, 15% modified wet distillers grains with solubles, and 10% supplement. For each block, total collection of feed, orts, feces and urine were conducted for two 5 d sampling periods during week 2 and 4 of RAC supplementation. No interaction (P > 0.21) between treatment and collection period was observed for any parameter evaluated. Dietary treatment had no effect (P = 0.51) on DMI, but RAC had decreased fecal DM output (P = 0.04) compared with CON. Thus, RAC had greater apparent total tract DM digestibility (77.2 vs. 73.5%; P < 0.01), N digestibility (72.4 vs. 69.4%; P = 0.01), and NDF digestibility (65.6 vs. 60.2%; P < 0.01) than CON. Although treatment did not affect nitrogen intake (P = 0.52), RAC tended to reduce total nitrogen excretion (113.3 vs. 126.7 g/d; P = 0.10) compared with CON due to a tendency for decreased fecal nitrogen output (53.9 vs. 61.3 g/d; P = 0.10). However, dietary treatment had no effect (P = 0.53) on urinary nitrogen output or percentage of urinary nitrogen excreted as urea (P = 0.28). Experiment 2 was an in vitro experiment conducted to validate the effects of RAC on nutrient digestibility using Simmental × Angus heifers (451 ± 50 kg). Rumen fluid was collected individually by stomach tube from CON- (n = 9) and RAC-fed (n = 10) heifers to inoculate bottles containing a CON or RAC-containing substrate in a split-plot design. No interaction between rumen fluid source and in vitro substrate was observed. Greater IVDMD (P = 0.01) was observed in rumen fluid from RAC-fed heifers compared with rumen fluid from CON-fed heifers. Inclusion of RAC in the in vitro substrate increased IVDMD (P < 0.01). Overall, feeding RAC increased microbial digestion of the dry-rolled corn-based finishing diet to increase total tract dry mater digestion by 5% and reduce nitrogen excretion by 10.6% in the 35 d period prior to slaughter.

PROTEINASE-INHIBITOR COMPLEXES (PIC) IN SEPTIC AND NON-SEPTIC SHOCK. COAGULATION; LEUKOCYTE AND BACTERIAL PROTEASE INHIBITION BY MEANS OF PLASMA-INHIBITOR REPLACEMENT

1987 ◽  
Author(s):  
R Egbring ◽  
R Seitz ◽  
M Wolf ◽  
L Lerch ◽  
T Menges
Keyword(s):  
Antithrombin Iii ◽  
Coagulation Factors ◽  
In Vitro Models ◽  
Protease Inhibition ◽  
E Coli ◽  
Bacterial Protease ◽  
Bacterial Endotoxins ◽  
At Iii ◽  
Cardiac Shock

In septic or cardiac shock antithrombin III-thrombin (AT III-Thr) and a1antitrypsin-elastase(a1AT-ELP) as well as a2antiplas-min-plasmin (a2AP-Pl) are found to be elevated to different extents. In cardiac shock AT III-Thr is predominantly increased, while in septic disorders a2AT-ELP as indicator of leukocyte stimulation is additionally found to be elevated. Stimuli for leukocyte activation are bacterial endotoxins, immune complexes, factor Xlla and others. The possible action of bacterial proteases during septic infections is only known in animal models. To stop hemorrhagic complications in disseminated intravascular coagulation (DIC) following septic (n=24) or non-septic (n=15) shock, we treated the patients with AT III concentrate and FFP in relatively high amounts containing a2macroglobulin (a2M), a1antitrypsin (a1AT) and others which are not available as concentrates. Subsequent to the procedure PIC's decreased, coagulation factors and inhibitors as well as thrombocyte counts increased. In in vitro models bacterial proteases have been shown to destroy a1AT, activate prothrombin and others. Only a2M may inhibit proteolytic activity of Staph aureus, N. meningitidis, P. aeroginosa and K1. pneumoniae and E. coli as our in vitro studies, using fibrin plates containing a2M, demonstrated. Not only bleeding or microthrombotic complications might be influenced by plasma derivative substitution, but also proteases released from bacteria

Resistance to whole-body X-irradiation in rats made tolerant to bacterial endotoxins

1959 ◽  
Vol 197 (6) ◽  
pp. 1364-1370 ◽  
Author(s):  
B. W. Zweifach ◽  
E. Kivy-Rosenberg ◽  
Arnold L. Nagler
Keyword(s):  
Blood Platelet ◽  
Reticuloendothelial System ◽  
Whole Body ◽  
X Rays ◽  
Effective Protection ◽  
X Ray ◽  
E Coli ◽  
Bacterial Endotoxins ◽  
X Irradiation ◽  
Reticulo Endothelial System

Rats were treated with three conditioning agents (bacterial endotoxins, zymosan and compound 48/80) known to produce tolerance to other forms of stress, as a means of determining the importance of the reticulo-endothelial system in the response to WBR. Effective protection was provided by tolerance induced by lipopolysaccharide extracts of E. coli bacteria. Some protection was also afforded by conditioning with 48/80 for several days. These agents were active only when administered before exposure to x-rays. Treatment post x-ray broke down the induced resistance. Blood platelet levels remained high in conditioned animals exposed to WBR. It is suggested that a relationship exists between the priming or conditioning of the reticuloendothelial system and the maintenance of satisfactory blood platelet levels in adapted animals receiving WBR.

scholarly journals Suppression of in vitro antibody response by a serum factor (SAA) in experimentally induced amyloidosis.

1975 ◽  
Vol 142 (1) ◽  
pp. 236-241 ◽  
Author(s):  
M D Benson ◽  
M A Aldo-Benson ◽  
T Shirahama ◽  
Y Borel ◽  
A S Cohen
Keyword(s):  
Antibody Response ◽  
Amyloid Fibrils ◽  
Amyloid Fibril ◽  
Normal Serum ◽  
Major Constituent ◽  
Mouse Serum ◽  
Serum Factor ◽  
Chronic Antigenic Stimulation ◽  
Amyloid Fibril Protein

Serum from CBA/J mice made amyloidotic by chronic casein injections has been shown to suppress in vitro antibody response to SRBC. Similar suppression was also found with normal mouse serum but to a much lesser degree. This suppressive activity of both amyloidotic serum and normal serum was removed by absorption of the sera with antiserum to protein AA, the major constituent of casein-induced (secondary) amyloid fibrils. This antiserum to the amyloid fibril protein AA (mol wt 8,400 daltons) detects an immunologically cross-reacting serum alpha globulin (SAA) (mol wt approx. 100,000). It is postulated that the serum factor (SAA) is a regulator of antibody response and may be present in elevated amounts as the result of chronic antigenic stimulation.

scholarly journals Evidence that interleukin-6 does not play a role in the stimulation of platelet production after induction of acute thrombocytopenia

Blood ◽  
1992 ◽  
Vol 80 (2) ◽  
pp. 346-351 ◽  
Author(s):  
RJ Hill ◽  
MK Warren ◽  
J Levin ◽  
J Gauldie
Keyword(s):  
Interleukin 6 ◽  
Protein A ◽  
Normal Serum ◽  
Mouse Serum ◽  
Severe Thrombocytopenia ◽  
Prolonged Administration ◽  
Maturation In Vitro ◽  
Heterologous Serum ◽  
Stimulation Of

Abstract The induction of thrombocytopenia results in elevated levels of thrombopoietin (TPO), which can be detected in the plasma of experimental animals. Acute, severe thrombocytopenia (platelet count less than 5% of control) was produced in mice by the administration of either guinea pig or rabbit antimouse platelet antiserum. Control mice received equal volumes of normal serum. At various times after the induction of thrombocytopenia (0.5, 1, 2, 3, 4, 6, 12, and 24 hours) citrated plasma was collected, and circulating interleukin-6 (IL-6) levels were measured using the IL-6-dependent murine hybridoma cell line B9. At no time points after induction of thrombocytopenia were plasma IL-6 levels significantly different from control animals that received normal serum. However, injection of heterologous serum did result in slightly elevated plasma IL-6 levels (at 2 and 3 hours) compared with basal levels measured in uninjected animals. This brief increase was not related to the production of thrombocytopenia. Protein fractions from the plasma of thrombocytopenic rabbits were also tested for the presence of IL-6. Preparations that contained TPO, as shown by stimulation of megakaryocyte maturation in vitro, did not contain detectable levels of IL-6. The ability of the B9 assay to detect the elevation of IL-6 levels in murine or rabbit plasma was verified after the administration of bacterial endotoxin, which is known to increase circulating IL-6 concentrations. IL-6 levels were highly elevated in rabbit or mouse serum after the administration of 5 mg/kg or 1 mg/kg of endotoxin, respectively. Anti-IL-6 antiserum did not neutralize the in vitro megakaryocyte maturation activity of partially purified TPO from the plasma of thrombocytopenic rabbits. In addition, IgG purified from the same antiserum did not neutralize partially purified TPO, as shown after incubation with TPO and subsequent precipitation with agarose- bound protein A. These results show that, unlike TPO, levels of IL-6 do not increase after the induction of acute, severe thrombocytopenia, and strongly suggest that IL-6 does not mediate the thrombopoietic response to acute thrombocytopenia. Although prolonged administration of IL-6 has been shown to induce thrombocytosis, IL-6 and TPO are apparently different and immunologically distinct molecules.

scholarly journals In-Vitro and In-Vivo Tolerance and Therapeutic Investigations of Phyto-Fabricated Iron Oxide Nanoparticles against Selected Pathogens

Toxics ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 105
Author(s):  
Amreen Shah ◽  
Isfahan Tauseef ◽  
Manel Ben Ali ◽  
Muhammad Arfat Yameen ◽  
Amine Mezni ◽  
...  
Keyword(s):  
Iron Oxide ◽  
Iron Oxide Nanoparticles ◽  
Severe Infection ◽  
Oxide Nanoparticles ◽  
Mice Model ◽  
Desorption Process ◽  
X Ray ◽  
E Coli

The Paeonia emodi (P. emodi)-mediated iron oxide nanoparticles (Fe2O3 NPs) were screened for in-vitro and in-vivo antibacterial activity against the Staphylococcus aureus (S. aureus) (ATCC #: 6538) and Escherichia coli (E. coli) (ATCC #:15224). The synthesized Fe2O3 NPs were characterized via nitrogen adsorption-desorption process, X-ray diffractometer (XRD), transmission and scanning electron microscopies (TEM and SEM), energy dispersive X-ray (EDX) and Fourier transform infrared (FTIR) spectroscopies. The SBET was found to be 94.65 m2/g with pore size of 2.99 nm, whereas the average crystallite and particles size are 23 and 27.64 nm, respectively. The 4 μg/mL is the MIC that inhibits the growth of E. coli, whereas those for S. aureus are below the detection limit (<1.76 μg/mL). The tolerance limit of the mice model was inspected by injecting different concentration of Fe2O3 NPs and bacteria suspensions. The 14 ppm suspension was the tolerated dose and the concentration above were proved lethal. The most severe infection was induced in mice with injection of 3 × 107 CFUs of both bacteria, while the inoculation of higher concentrations of bacterial suspensions resulted in the mice’s death. The histopathological and hematological studies reveals that the no/negligible infection was found in the mice exposed to the simultaneous inoculation of Fe2O3 NPs (14 ppm) and bacterial suspensions (3 × 107 CFUs).

scholarly journals EFFECTS OF BACTERIAL ENDOTOXINS ON METABOLISM

1961 ◽  
Vol 114 (5) ◽  
pp. 761-778 ◽  
Author(s):  
L. Joe Berry ◽  
Dorothy S. Smythe
Keyword(s):  
Adrenal Glands ◽  
Nitrogen Excretion ◽  
Maximal Response ◽  
In Vitro Tests ◽  
Phenol Red ◽  
Experimental Conditions ◽  
Protein Nitrogen ◽  
Urinary Nitrogen Excretion ◽  
Urinary Nitrogen

In vitro secretion of glycocorticoids by adrenal glands pooled from several control mice was compared with that of glands removed from animals following injections of either ACTH or endotoxin. Both substances prevent glycocorticoid synthesis stimulated in vitro with ACTH. Cholesterol content of adrenal glands under these conditions was nearly depleted, indicating maximal response to ACTH or endotoxin prior to their removal for the in vitro tests. In an effort to account physiologically for the manner in which endotoxin suppresses or prevents the rise in urinary nitrogen excreted in response to ACTH, blood non-protein nitrogen levels (NPN) were determined. The following experimental conditions resulted in increased urinary nitrogen excretion but did not alter blood NPN: cortisone given alone or at the same time as endotoxin; ACTH alone; dichloroisoproterenol (DCI) given concurrently with endotoxin; and lactalbumin digest injected intraperitoneally. Increases (2- to 3-fold) in blood NPN were observed when endotoxin was given alone, concurrently with ACTH, or 3 hours prior to cortisone, DCI, or lactalbumin digest. Urinary nitrogen excretion showed no change under these conditions. The elevation in blood NPN in endotoxin-poisoned mice was found to be due almost entirely to urea nitrogen and not to amino acid nitrogen or to other nitrogenous wastes. Blood clearance of mulin, phenol red excretion, and urea elimination were each determined in control and in endotoxin-poisoned mice. The latter mice showed impaired renal function. Treatment with diuretics (diuril and aminophylline) failed to alter oliguria or elevated blood NPN. Hydergine treatment was also without effect. Total carcass NPN and urinary nitrogen excretion data were combined to give a picture of total protein catabolized by mice under different experimental conditions. Cortisone injected at the same time as endotoxin or 3 hours later resulted in the same increase in total NPN. However, in the former case all the extra nitrogen appeared in the urine while in the latter it remained in the carcass. ACTH given alone or concurrently with endotoxin produced large increases in total NPN but less in poisoned mice. This suggests that endotoxin suppresses adrenal response to ACTH. Urea injected into normal mice was recovered quantitatively in urine while in endotoxin-poisoned mice it was partitioned between carcass and urine. Elevation of carcass NPN by means of urea injections failed to alter the lethality of an LD70 dose of endotoxin.

scholarly journals Effects of normal mouse serum on the IL-3-induced proliferation of bone marrow cells

Blood ◽  
1989 ◽  
Vol 73 (3) ◽  
pp. 700-705 ◽  
Author(s):  
CA Dahl ◽  
C Lindqvist
Keyword(s):  
Bone Marrow ◽  
Colony Formation ◽  
Normal Mouse ◽  
Bone Marrow Cells ◽  
Normal Serum ◽  
Mouse Serum ◽  
Mouse Bone Marrow ◽  
Normal Mouse Serum ◽  
High Concentrations

Abstract Normal mouse serum (NMS) devoid of colony-stimulating factor (CSF) was found to enhance the interleukin 3 (IL-3)-driven colony formation of bone marrow in vitro. Inclusion of NMS in bone marrow colony-forming assays resulted in greatly increased numbers of colonies and clusters following seven days incubation; however, incubation of bone marrow with NMS before the colony-forming assay had no effect on resultant colony number. The levels of serum-enhancing activity (SEA) did not appear to vary significantly with age and in part was species restricted, in that human and guinea pig serum did not enhance mouse bone marrow colony formation. Conversely, NMS had no effect on human bone marrow colony formation. Levels of SEA were found to vary between strains, as did the degree to which bone marrow from various strains was enhanced by the serum. Serum fractionation studies indicated three active fractions with molecular weights of 800–900 Kd, 60–70 Kd, and 20- 30 Kd. The fraction at 800–900 Kd inhibited colony formation at high concentrations and enhanced colony formation on dilution, whereas the two other active fractions contained enhancing activity at all concentrations tested. These results would indicate that normal serum can play a greater role in colony-forming assays than nutritional supplements. The relationship of the SEA factors to other factors that have been reported to modulate bone marrow colony formation is discussed.

scholarly journals Effects of normal mouse serum on the IL-3-induced proliferation of bone marrow cells

Blood ◽  
1989 ◽  
Vol 73 (3) ◽  
pp. 700-705 ◽  
Author(s):  
CA Dahl ◽  
C Lindqvist
Keyword(s):  
Bone Marrow ◽  
Colony Formation ◽  
Normal Mouse ◽  
Bone Marrow Cells ◽  
Normal Serum ◽  
Mouse Serum ◽  
Mouse Bone Marrow ◽  
Normal Mouse Serum ◽  
High Concentrations

Normal mouse serum (NMS) devoid of colony-stimulating factor (CSF) was found to enhance the interleukin 3 (IL-3)-driven colony formation of bone marrow in vitro. Inclusion of NMS in bone marrow colony-forming assays resulted in greatly increased numbers of colonies and clusters following seven days incubation; however, incubation of bone marrow with NMS before the colony-forming assay had no effect on resultant colony number. The levels of serum-enhancing activity (SEA) did not appear to vary significantly with age and in part was species restricted, in that human and guinea pig serum did not enhance mouse bone marrow colony formation. Conversely, NMS had no effect on human bone marrow colony formation. Levels of SEA were found to vary between strains, as did the degree to which bone marrow from various strains was enhanced by the serum. Serum fractionation studies indicated three active fractions with molecular weights of 800–900 Kd, 60–70 Kd, and 20- 30 Kd. The fraction at 800–900 Kd inhibited colony formation at high concentrations and enhanced colony formation on dilution, whereas the two other active fractions contained enhancing activity at all concentrations tested. These results would indicate that normal serum can play a greater role in colony-forming assays than nutritional supplements. The relationship of the SEA factors to other factors that have been reported to modulate bone marrow colony formation is discussed.

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