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At least 19 recordsLinked to original sources
PubMed1989

Effect of dichloroacetate on plasma and hepatic amino acids in sterile inflammation and sepsis.

The effect of sterile inflammation and chronic sepsis on the plasma and hepatic free amino acid concentrations was determined. Relative to control animals, only minor alterations in the plasma amino acid concentrations were observed in sterile inflammation and sepsis. In liver, concentrations of alanine, serine, threonine, asparagine, proline, and glycine were significantly increased to the same extent in sterile inflammation and sepsis, while hepatic glutamine concentrations were significantly decreased. Compared with sterile inflammation, the branched-chain amino acid concentrations were depressed in the liver of septic animals. Following administration of dichloroacetate, hepatic alanine concentrations were significantly reduced more than threefold in each of the conditions examined; in contrast, significant increases in hepatic concentrations of threonine, glycine, glutamine, glutamate, histidine, and proline were observed. Also following administration of dichloroacetate, the branched-chain amino acid concentrations were all significantly elevated in each of the conditions examined, and plasma alanine concentrations were significantly decreased, while those of glutamine and glycine were significantly increased. These results demonstrate that there is a disassociation between the plasma and hepatic concentration of free amino acids in sterile inflammation and sepsis. Furthermore, the results demonstrate that some of the alterations in hepatic amino acid metabolism may be reversed pharmacologically by dichloroacetate.

Abscess↗
PubMed1998

The kinetics of radiolabelled interleukin-8 in infection and sterile inflammation.

Radiolabelled interleukin-8 (IL-8) is a promising agent for the imaging of infection and inflammation. Several experiments were performed to explore further the imaging potential of radiolabelled IL-8. IL-8 was radioiodinated via the Bolton-Hunter method. Rabbits with focal infection (Escherichia coli, Staphylococcus aureus) or sterile inflammation (zymosan) were injected intravenously with 18.5 MBq (0.5 mCi) of 123I-IL-8. In separate studies, rabbits were injected intravenously with 111In-granulocytes with or without 125I-IL-8. Gamma camera images were obtained at 5 min, 1, 4 and 8 h post-injection (p.i.). Biodistribution was determined at 8 h p.i. In all models, the biodistribution of 123I-IL-8 was characterized by rapid blood clearance and high uptake in infection and sterile inflammation. All foci could be clearly visualized within 4 h p.i. Ex vivo abscess-to-contralateral muscle ratios increased to 114.7+/-23.0 (E. coli), 52.3+/-24.5 (S. aureus) and 49.8+/-8.3 (zymosan) at 8 h p.i. In the circulation, most 123I-IL-8 was bound to erythrocytes. The abscess uptake of 125I-IL-8 reached high levels despite reduced migration of granulocytes towards the site of infection due to the anti-inflammatory activity of intravenously injected IL-8. IL-8 could be injected without induction of neutropenia at a dosage of 2 ng kg(-1). In conclusion, the characteristics of radiolabelled IL-8 for imaging of infection and sterile inflammation are highly encouraging and warrant further optimization for clinical application.

Animals↗
PubMed1993

Stimulator of proliferation of spleen colony-forming cells in acute sterile inflammation.

The presence and activity of a spleen colony-forming cell (CFU-S) proliferation stimulator was investigated in rat bone marrow after induction of sterile inflammation. Wistar rats were treated intraperitoneally with two 15 ml injections of 3.5% polyvinylpyrrolidone (PVP) at 18 h intervals, and the presence of CFU-S proliferation stimulator determined in bone marrow 6, 20 and 24 h after the first injection. The marrow of these mice was used to condition medium which was then fractionated using Amicon Diaflo ultrafiltration membranes. The 30-50 kDa fraction, taken from 20h post-PVP-bone marrow extract, was found to induce cycling of d8-CFU-S in normal mouse bone marrow. This activity was not related to the presence of interleukins-1, -2 or -6 like activities in the material tested. The results demonstrate the existence of CFU-S proliferation stimulator in the bone marrow of rats with sterile inflammation (i.e. in an in vivo tissue response to non-specific cell stimulation), similar to that originally described as a macrophage product in mouse bone marrow after treatment with a variety of cytotoxic agents.

Animals↗
PubMed1997

Technetium-99m-labeled chemotactic peptides in acute infection and sterile inflammation.

UNLABELLED: Chemotactic peptides have been proposed as vehicles to image infection and inflammation. Previous studies have shown high uptake at the site of infection soon after injection, most likely because of specific binding to receptors on locally present leukocytes. To investigate this hypothesis, the in vivo behavior of a synthetic chemotactic peptide was compared to a control peptide of similar molecular weight with low receptor binding affinity. In addition, the potential to target to different infections and sterile inflammation was tested. METHODS: Twenty-four hours after induction of Escherichia coli, Staphylococcus aureus and zymosan abscesses, rabbits were i.v. injected with either 1 mCi of 99mTc-labeled formyl-methionyl-leucyl-phenylalanyl-lysine-hydrazinonicotinamid e (99mTc-fMLFK-HYNIC) or 99mTc-labeled hydrazinonicotinamide-methionyl-leucyl-phenylalanyl-OMe (99mTc-HYNIC-MLFOMe, control peptide). Gamma camera images were obtained at 5 min and 1, 4, 8 and 20 hr postinjection. Biodistribution was determined at 20 hr postinjection. RESULTS: The blood clearances of 99mTc-fMLFK-HYNIC and 99mTc-HYNIC-MLFOMe were similar. With time, 99mTc-fMLFK-HYNIC was retained in the abscess (E. coli), whereas the control agent 99mTc-HYNIC-MLFOMe was cleared from the abscess (0.049 +/- 0.011 versus 0.005 +/- 0.0003% 1D/g at 20 hr postinjection; p < 0.0005). Abscess-to-contralateral muscle ratios of 99mTc-fMLFK-HYNIC rose to 36.8 +/- 4.3 at 20 hr postinjection. E. coli, S. aureus and zymosan abscesses were clearly visualized from 4 hr postinjection onward. Abscess-to-background ratios increased to values varying from 4.4 +/- 0.2 (zymosan) to 7.1 +/- 0.6 (S. aureus) at 20 hr postinjection. The uptake in S. aureus and zymosan abscesses did not differ significantly from the uptake in E. coli abscesses. CONCLUSIONS: fMLFK-HYNIC is retained in both acute infection and sterile inflammation by means of specific receptor binding if sufficient cellular infiltration is present.

Abscess↗
PubMed1993

Acute sterile inflammation--correlation between cellular changes and extramedullary-produced regulators in vivo.

Rats with polyvinylpyrrolidone (PVP)-induced sterile inflammation were used as a model in vivo for investigation of granulopoiesis and extramedullary-produced regulators. The data obtained demonstrated the invasion of massive numbers of granulocytes at the site of inflammation (peritoneal cavity) during the first 24 h of the acute phase of inflammation. To meet the organism's needs for granulocytes the activation of granulopoiesis in bone marrow occurred simultaneously. Accelerated production of granulocytic cells is manifested by involvement of granulocytic proliferative compartment in various stages of differentiation (CFU-GM and morphologically recognizable proliferative granulocytes--PG). Together with cellular changes within the granulocytic cells line, the changes in the content of investigated regulators influencing granulopoiesis were observed. At different time intervals the levels of interleukin-6 (IL-6), colony-stimulating activity (CSA), and granulocytic stimulating activity (GSA) were increased locally at the site of inflammation as well as in serum. The data obtained provide evidence that inducible granulopoiesis during the acute phase of inflammation is under the control of extramedullary-produced regulators, thus confirming their role in the regulation of granulocytic production in vivo.

Animals↗
PubMed1977

Changes in the concentration of leucocytes and platelets in the peripheral blood during sterile inflammation in rabbits.

Glycogen in isotonic saline was infused into the peritoneal cavities of rabbits to produce sterile inflammation. This caused a small increase in the haematocrit value and larger decreases in the concentrations of circulation leucocytes and platelets. Circulating granulocytes decreased by about 40% in 2 h and increased in the next 2 h to about 4 times their initial concentration. Acetyl salicyclic acid (ASA) (10 mg/kg) infused with the glycogen did not affect the decrease significantly but accelerated the subsequent increase. Circulating mononuclear leucocytes, mostly lymphocytes, decreased progressively by about 75% after 4-5 h. This decrease was not affected by ASA. Circulating platelets decreased by about 30% in the first hour; this decrease was accelerated and augmented by ASA. Subsequently the platelet concentrations remained constant for at least 4-5 h. Glycogen so infused is known to activate complement, and ASA to inhibit prostaglandin synthetase. Therefore the results suggest that (i) the initial decrease in circulating granulocytes is mediated by activated complement; (ii) the emigration of granulocytes from blood into the inflammatory exudate is increased by prostaglandins; (iii) the initial decrease in circulating platelets is mediated by activated complement and antagonized by prostaglandins; and (iv) the decrease in circulating lymphocytes is mediated by activated complement and uninfluenced by prostaglandins.

Animals↗
PubMed2000

Technetium-99m labelled antimicrobial peptides discriminate between bacterial infections and sterile inflammations.

The aim of this study was to select technetium-99m labelled peptides that can discriminate between bacterial infections and sterile inflammations. For this purpose, we first assessed the binding of various 99mTc-labelled natural or synthetic peptides, which are based on the sequence of the human antimicrobial peptide ubiquicidin (UBI) or human lactoferrin (hLF), to bacteria and to leucocytes in vitro. In order to select peptides that preferentially bind to bacteria over host cells, radiolabelled peptides were injected into mice intraperitoneally infected with Klebsiella pneumoniae (K. pneumoniae) and the amount of radioactivity associated with the bacteria and with the leucocytes was quantitated. The next phase focussed on discrimination between bacterial infections and sterile inflammatory processes using 99mTc-labelled peptides in mice intramuscularly infected with various bacteria (e.g. multi-drug-resistant Staphylococcus aureus) and in animals that had been injected with lipopolysaccharides (LPS) of bacterial origin to create a sterile inflammatory process. Also, we studied the distribution of 99mTc-labelled UBI 29-41 and UBI 18-35 in rabbits having an experimental thigh muscle infection with K. pneumoniae and in rabbits injected with LPS. Based on the results of our in vitro and in vivo binding assays, two peptides, i.e. UBI 29-41 and UBI 18-35, were selected as possible candidates for infection imaging. The radiolabelled peptides can detect infections with both gram-positive and gram-negative bacteria in mice as early as 5-30 min after injection, with a target-to-non-target (T/NT) ratio between 2 and 3; maximum T/NT ratios were seen within 1 h after injection. In rabbits, high T/NT ratios (>5) for 99mTc-labelled UBI 29-41 were observed from 1 h after injection. No accumulation of the selected 99mTc-labelled UBI-derived peptides was observed in thighs of mice and rabbits previously injected with LPS. Scintigraphic investigation into the biodistribution of 99mTc-labelled UBI peptides revealed that these peptides were rapidly removed from the circulation by renal excretion. Similar data were observed for 99mTc-labelled defensin 1-3. Our data for 99mTc-labelled hLF and related peptides indicate that these compounds are less favourable for infection detection. Taken together, 99mTc-labelled UBI 18-35 and UBI 29-41 enable discrimination between bacterial infections and sterile inflammatory processes in both mice and rabbits. Based on their characteristics, we consider these peptides the candidates of preference for detection of bacterial infections in man.

Animals↗
PubMed1998

The influence of acute sterile inflammation on erythropoiesis in rats.

Many different cell types, coordinated by proinflammatory mediators, take part in the acute inflammatory reaction, but there is a lack of evidence regarding the role of erythroid cells in such conditions. In this study, changes in bone marrow, splenic, and peripheral blood erythroid cells and in erythropoietin (Epo) blood levels were investigated up to 72 hours after polyvinylpyrrolidone (PVP)-induced sterile inflammation in male Wistar rats (two intraperitoneal injections of 15 mL 3.5% PVP at 18-hour intervals). Transient changes within progenitor erythroid cells were observed in the bone marrow. Significant increases in the number of splenic immature erythroid progenitors (BFU-E) 6 hours and mature erythroid progenitors (CFU-E), erythroblasts, and orthochromatic erythroblasts 48 and 72 hours after the induction of inflammation pointed to stimulated splenic erythropoiesis. This was confirmed by semiquantitative assessment of splenic smears, which demonstrated expansion of erythroid cells at hours 48 and 72. The changes observed in the bone marrow and spleen indicated that during acute inflammation erythropoiesis was stimulated and that the spleens of PVP-treated rats were favorable to erythroid development. The significant increase in the percentage of peripheral blood reticulocytes 48 and 72 hours after PVP-induced inflammation provided evidence that effective erythropoiesis occurred. In spite of the stimulated erythropoiesis, serum levels of Epo remained unchanged, implying that other non-Epo regulatory molecules may be responsible for erythroid cellular changes.

Acute Disease↗
PubMed1986

The effect of sterile inflammation on skin flap survival.

Several investigations have suggested that a sterile inflammatory reaction in a skin flap enhances flap survival. A chemical peel produces a mild chemical burn, which is one form of nonbacterial inflammatory response. Some authors advocate the concomitant use of face lift and chemical peel, while others caution that the peel might jeopardize the facial flaps. To determine whether the reaction caused by a chemical peel enhances or impairs skin flap survival, a study using miniature pigs was undertaken. Survival length of flaps treated with a chemical peel was compared to that of untreated flaps. A total of 36 dorsally based random flaps were used on three miniature pigs. Six identical 14 X 4 cm flaps were designed on each side of the pigs. A chemical peel was applied to the area of 18 of the proposed flaps 2 days prior to elevation. Alternate flaps on each side of the pigs were treated. As the flaps were elevated, the tips were examined to document the inflammatory response histologically. After 14 days, the surviving length of the flaps was measured. As determined by the Wilcoxon matched-pairs signed-ranks test, there was no significant difference between the treated and untreated groups. Our study shows that a nonbacterial inflammatory response produced by a chemical peel does not improve skin flap survival, at least not in pigs.

Animals↗
PubMed2003

Sterile inflammation associated with transradial catheterization and hydrophilic sheaths.

In 1999, we noted the development of inflammation and/or abscesses at the site of radial access in a group of patients. Over a 3-year period, we noted this inflammation in 33 patients out of 2,038 (1.6%) who had catheterization via the radial approach. The radial abscesses occurred in 30 patients out of 1,063 (2.8%) in whom we could confirm the use of a hydrophilic-coated sheath, but in no patient for whom we can document that an uncoated sheath was used. No infectious agent could be implicated, and the time course for the development of the abscess, typically 2 to 3 weeks, seemed long for a bacterial infection. Later patients had biopsies, and granulomatous reactions were seen in most. Additionally, a few of the biopsies showed an amorphous extravascular substance consistent with the catheter coating. All patients had good long-term outcomes.

Abscess↗
PubMed1994

Effects of antifungal therapy on inflammation, sterilization, and histology in experimental Candida albicans meningitis.

To assess the effects of antifungal therapy on the course of Candida albicans central nervous system infection and inflammation, we inoculated intracisternally 10(5) CFU of C. albicans into rabbits. Fluconazole (10 mg/kg of body weight) or amphotericin B (1 mg/kg) was infused intravenously daily for 14 days. Treatment was initiated 24 h or 5 days after infection. Cerebrospinal fluid (CSF) was repeatedly obtained to culture the organisms, assess the level of inflammation, and measure drug concentrations. Brain tissue was obtained at the end of therapy for culture, drug concentration determinations, and histopathology. The median number of days of treatment required to sterilize CSF cultures was 4 days for fluconazole therapy and 1 day for amphotericin B therapy (P = 0.037). There was a significant reduction in tumor necrosis factor alpha and leukocyte concentrations in the CSF of animals treated early versus those in untreated control animals (P < 0.05 and P < 0.001, respectively; analysis of variance). Compared with treated animals, a higher proportion of cultured CSF samples from untreated animals were positive for Candida (P < 0.001). A cultured brain sample from 1 of the 12 animals treated early with amphotericin B was positive for C. albicans (P < 0.01 versus controls); cultures of brain samples from 3 of 12 animals treated early with fluconazole were positive, whereas cultures of brain samples from 10 of 12 controls were positive (P < 0.05). The mean density of C. albicans was lower in the single culture-positive amphotericin B recipient (1 x 10(1) CFU/g of brain tissue) than in those treated with fluconazole (1 x 10(3) CFU/g) and in controls (8 x 10(4) CFU/g). In animals treated late, the density of C. albicans in the brain in relation to the number of days of therapy was significantly lower in amphotericin B recipients than in those treated with fluconazole (P < 0.01) and untreated controls (P < 0.01; analysis of covariance). By histopathology, a larger proportion of untreated animals compared with those treated early demonstrated features of severe infection such as perivasculitis, ventriculitis, and evidence of fungal organisms. Compared with amphotericin B-treated rabbits, those given fluconazole had a trend toward more severe pathologic lesions. Reduced susceptibility to both fluconazole and amphotericin B was observed in the C. albicans organisms isolated from the brain of one fluconazole-treated animal. These data suggest that amphotericin B is the preferred treatment for C. albicans infections of the central nervous system.

Amphotericin B↗
PubMed1987

Intestinal iron absorption during turpentine sterile inflammation in the rat. Influences of isoproterenol and propranolol.

59Fe was incorporated in vivo into intestinal sacs prepared in control rats as well as in animals with turpentine sterile abscesses and 59Fe counts were detected in the intestinal wall, in blood, in liver, in spleen and in femur of animals, at different time intervals (20, 40 and 120 min) following i.v. injection of isoproterenol (10 micrograms/kg, body weight) or of (-)-propranolol (2 mg/kg, body weight). In rats without inflammation isoproterenol alone enhanced significantly iron counts in blood, spleen, liver and femur, but not in intestinal cells, whereas propranolol evoked opposite actions, the influence being more marked after 40 min, reaching maximal values at 120 min. In animals with sterile turpentine abscesses explored 40 min after injections, iron intestinal counts in turpentine, in turpentine plus isoproterenol and in turpentine plus propranolol groups were significantly lower than in normal saline injected controls (p less than 0.001) and the opposite was the case at 120 min. In blood, iron counts at 20 and 40 min were higher in saline controls (p less than 0.05) than in the turpentine group, whereas at 120 min, values in the turpentine plus isoproterenol group were higher than (p less than 0.01) in saline injected controls or in the group with turpentine alone. Also, at all time intervals explored, iron counts in blood in the propranolol plus turpentine group were smaller (p less than 0.01) than in saline injected controls or in the group with turpentine alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Hepatic gene expression and cytokine responses to sterile inflammation: comparison with cecal ligation and puncture sepsis in the rat.

Inflammatory stimulation of hepatic acute phase protein expression is, in part, modulated by tumor necrosis factor-alpha (TNFalpha), interleukin-1beta (IL-beta), and IL-6. These cytokines also may mediate some aspects of the persistent inflammation and metabolic dysregulation of sepsis. Cecal ligation and puncture (CLP) sepsis in male Sprague-Dawley rats inappropriately decreases hepatocellular transcription of phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphatase (G6Pase), carnitine palmitoyltransferase II (CPTII), acetyl CoA acyltransferase (ACA), and ornithine transcarbamylase (OTC). We hypothesize that 1) transcriptional reprogramming does not occur after simple inflammation induced by subcutaneous turpentine injection, 2) the pattern of acute phase gene expression after CLP differs from that following turpentine injection, and 3) the different responses reflect differences in the intrahepatic activity of TNFalpha/IL-1beta or IL-6. Gene expression, transcription factor activity, and cytokine abundance were determined after either a subcutaneous injection of turpentine or CLP. After turpentine injection, PEPCK, G6Pase, CPTII, ACA, and OTC expression were unchanged, different from previously reported data following CLP. Both turpentine injection and CLP increased expression of TNFalpha/IL-1beta-regulated alpha1-acid glycoprotein, and IL-6-regulated alpha2-macroglobulin and decreased expression of transthyretin (a negative acute phase protein). However, the magnitude and temporal pattern of expression differed. Turpentine injection increased the activity of the TNFalpha/IL-1beta-linked transcription factor NF-kappaB and the intrahepatic abundance of TNFalpha in a manner similar to that observed after CLP but only slightly altered the activity of the IL-6-linked transcription factor Stat-3 and intrahepatic IL-6 abundance. This differed significantly from observations after CLP. We conclude that CLP-induced alterations in hepatic gene expression may reflect differences in IL-6 activity.

Acute-Phase Reaction↗
PubMed1989

Action of blood serum from rats with turpentine sterile inflammation on the development of CFU erythrocyte colonies. Possible role of erythropoietin.

Bone marrow CFUe mice cultures were prepared in Petri dishes and the number of full developed erythrocyte colonies were counted under various experimental conditions. In certain experiments, erythropoietin (EP = 0.4 U x ml-1 in the suspending medium) or sera from normal rats (100 microliters) or from animals with chronic turpentine sterile abscesses (60 or 100 microliters), were delivered to the CFUe colonies. The number of colonies in the group without EP was almost 5 times smaller than in the group with EP. Inasmuch as some few colonies are still able to develop, even in absence of added EP, the suggestion is advanced holding that the phenomenon may represent the effect of EP already bound to the group of cells initiating differentiation. Comparisons among all experimental groups indicate that the delivery of sera from turpentine rats to cultures containing added EP, reduced significantly the number of CFUe colonies seen in controls with EP but without inflammatory serum. It is suggested that the present findings could be explained assuming an inhibition of the influence of exogenous EP, subserved by the inflammatory serum, or alternatively that this kind of rat serum induces a partial blockade of EP at receptor sites whose activation is a mandatory step for the adequate and full development of cultured erythrocytes.

Abscess↗
PubMed1990

The acute phase protein response in mice does not show tolerance to recurrent sterile inflammation.

The response of acute phase proteins to repeated inflammatory stimuli was studied in BALB/c mice and Hylyne Dutch rabbits. Inflammation was produced by subcutaneous injections of turpentine/arachis oil twice weekly for three and a half weeks. Serum amyloid-P component (SAP) levels in the mice showed no significant decrease in the level of response following each injection and the pattern of response was the same in mice previously rendered tolerant to endotoxin. Haptoglobin levels in the rabbits also responded equally to repeated injections in two animals and showed a declining response in a third animal which became unwell during the experiment. The ability of experimental animals to continue to respond fully to repeated inflammatory stimuli supports the suggestion that the subnormal responses seen in certain chronic inflammatory conditions may reflect an underlying defect in the acute phase response rather than an adaptive change following chronic inflammation.

Acute-Phase Proteins↗