UMLS:C0341503 - FACTA Search

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Query: UMLS:C0341503 (bacterial peritonitis)
1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normal mice exposed to 10% oxygen concentration developed a slight but statistically significant decrease in blood pH and a slight statistically insignificant decrease in red cell 2,3-DPG. Mice that were infected intraperitoneally with Staphylococcus aureus or Klebsiella pneumoniae and exposed to 20% oxygen developed acidosis, hemoconcentration, and decreased red cell 2,3-DPG levels. When mice with acute bacterial peritonitis were exposed to 10% oxygen concentration they likewise developed significant acidosis and hemoconcentration, but their reduction in red cell 2,3-DPG was not as great as that in the similarly infected mice exposed to 20% oxygen concentration.
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PMID:The effects of Staphylococcus aureus and Klebsiella pneumoniae peritonitis in mice exposed to normal and hypoxic conditions on red cell oxygen transport function. 23 91

Interferon-gamma (IFN-gamma) can be considered a primary factor required in vitro and in vivo for inducing endocellular lysis of microorganisms by peritoneal macrophages (PM luminal diameter), an essential activity in continuous ambulatory peritoneal dialysis (CAPD) patients that prevents bacterial peritonitis. In 22 uremic patients treated with CAPD we analyzed: (1) the amount of IFN-gamma released by elicited peritoneal lymphocytes (PL); (2) oxidative metabolism and microbicidal activity by elicited PM luminal diameter; (3) immunoglobulin G (IgG) Fc-receptor expression on PM luminal diameter membrane; (4) the effect on PM luminal diameter hydrogen peroxide (H2O2) generation, bactericidal activity, and IgG Fc-receptor expression exerted in vitro by human recombinant IFN-gamma (rIFN-gamma). Results demonstrate that IFN-gamma release by elicited PL is lower in some CAPD patients with high peritonitis incidence (HPI) than in healthy donors or in CAPD patients with low peritonitis incidence (LPI). Simultaneously, PM luminal diameter from CAPD patients with HPI are characterized by a decreased ability to generate oxygen metabolites, to kill bacteria, and by a lack in IgG Fc-receptor expression; these defects were completely cured after being treated with rIFN-gamma. These results show that the IFN-gamma treatment in vitro could strengthen PM luminal diameter phagocytosis, oxygen metabolite generation, and bacterial killing in CAPD patients with HPI, and suggest that IFN-gamma may be considered a possible therapy in vivo for these patients.
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PMID:Interferon-gamma (IFN-gamma) as in vitro enhancing factor of peritoneal macrophage defective bactericidal activity during continuous ambulatory peritoneal dialysis (CAPD). 312 40

Adenosine exhibits potent anti-inflammatory activities but its therapeutic use is limited by cardiovascular side effects. Inhibitors of an enzyme involved in adenosine metabolism, adenosine kinase (EC 2.7.1.20), were evaluated for their ability to enhance endogenous adenosine production. One novel adenosine kinase inhibitor, GP-1-515, was studied in two models of septic shock to assess its protective effects. GP-1-515 significantly decreased mortality in mice that received a lethal i.v. injection of endotoxin. The beneficial effect was accompanied by decreased neutrophil accumulation in the lungs and was reversed by an adenosine receptor antagonist, implying that the effects were mediated by endogenous adenosine. Plasma levels of TNF-alpha, but not IL-1 alpha or IL-6, were lower in the GP-1-515-treated animals. In a second model of sepsis, GP-1-515 increased survival in bacterial peritonitis in rats. The mechanism of action in both models was likely multifactorial, including adenosine-mediated inhibition of neutrophil adhesion, cytokine production, and oxygen radical generation. Adenosine kinase inhibitors have potent anti-inflammatory effects in vitro and in vivo and represent a novel therapeutic approach to the treatment of inflammatory diseases.
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PMID:Protective effect of an adenosine kinase inhibitor in septic shock. 820 12

We describe a case of spontaneous bacterial peritonitis in a 53 year old man affected by cryptogenic micro-macronodular cirrhosis, portal hypertention, splenomegaly and hypersplenism, who was admitted with hepatic failure and septic shock and successfully treated with antibiotics (combination of clindamycin and netilmycin), surgical abdominal drainage and splenectomy. This case gave reason for a literature review and an update on the therapeutic options in these high risk patients, especially concerning the role of surgery. Spontaneous Bacterial Peritonitis (SBP) is defined as a bacterial infection of ascitic fluid in the absence of any septic focus. It is a typical life-threatening complication of hepatic cirrhosis with ascites. Mortality is very high and ranges from 75% to 97% of patients, due to septic shock and hepatic failure (hepatorenal syndrome, hepatic encephalopathy, gastrointestinal bleeding). Infection with a single organism is found in most cases. Gram negative bacilli are present in about 70% of cases and E. coli (less frequently Klebsiella, Serratia, Pseudomonas) is principally found. Gram positive cocchi comprise an additional 30% of cases. Anaerobic and microaerophilic organisms seem to be rare causes of SBP (2.7-6%); this finding is probably due to the intrinsic bacteriostatic activity of ascites, which contains high oxygen tension (70 mmHg) and is an inhospitable environment for bacteroides and Clostridia. The prevalent isolation of enteric organism suggest that the gut is the most frequent source of infection, even if the pathogenetic mechanism is not yet well known. The right treatment depends on differentiating primary (SBP) from secondary peritonitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Is the surgical treatment of spontaneous bacterial peritonitis still up-to-date?]. 824 98

Erythrocytes (RBC) in the peritoneal cavity significantly increase the lethality of bacterial peritonitis. The lethality is known to be associated with, and perhaps due to, increased bacterial counts in the peritoneal cavity. The mechanism is unknown. In this study, we investigated the hypothesis that RBC scavenge reactive oxygen intermediates (ROI) and nitric oxide (NO), so that the counterprotective effect is due to a loss of the microbiostatic activity of both ROI and NO. To study this effect, rats were subjected to a peritoneal inoculation of live Escherichia coli without RBC (nonlethal dose) or with RBC (lethal dose). The adjuvant effect of RBC was not modified by NG-monomethyl-L-arginine (NMA, an NO synthase inhibitor), superoxide dismutase, catalase, mannitol, or a combination of these agents. Furthermore, the increased number of bacteria in the peritoneal cavity in the presence of RBC was unaffected by these treatments. The administration of NMA with bacteria alone (no RBC) converted a nonlethal model into a lethal one associated with higher intraperitoneal bacterial counts. A similar effect was seen with superoxide dismutase and catalase but not with mannitol. During bacterial peritonitis in the absence of RBC, superoxide and NO formation (determined by the total nitrite plus nitrate formed) was detected in the ascites and inducible NO synthase mRNA expression was present in the peritoneal cells. In the absence of RBC, superoxide was detected and oxidation of dihydrorhodamine to rhodamine was observed, indicating that peroxynitrite was produced. Both were blocked by the inclusion of RBC. Preinjection with a low inoculum of killed bacteria protected the rats from a subsequent lethal peritoneal bacterial challenge; this effect was reversed by scavenging ROI and NO. The protective effect of killed bacterial pretreatment was lost when RBC were placed in the peritoneal cavity. In vitro bactericidal activity of NO- and ROI-generating macrophages was also inhibited by RBC or by inhibiting ROI and NO formation. Taken together, these data are consistent with the hypothesis that RBC can impair bacterial clearance by removing both NO and ROI, suggesting that NO in combination with superoxide may be important to the antimicrobial defenses of the peritoneal cavity.
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PMID:Counterprotective effect of erythrocytes in experimental bacterial peritonitis is due to scavenging of nitric oxide and reactive oxygen intermediates. 875 36

Bacterial peritonitis is the most important complication of peritoneal dialysis (PD), limiting its widespread application. Conventional glucose-based peritoneal dialysates (G-PDS) depress oxygen consumption, chemiluminescence, superoxide production, phagocytosis, bacterial killing and actin polymerization in neutrophils (PMN) in vitro. Expression of adhesion receptors is critical to leukocyte activation, adhesion, migration and phagocytosis. The effects of G-PDS on basal and stimulated leukocyte adhesion molecule expression and leukocyte adhering capacity is unknown. We examined the effect of a five minutes incubation of whole blood in either HEPES-buffered saline or G-PDS containing 1.5% (83 mM), 2.5% (139 mM) or 4.25% (236 mM) glucose, at pH = 5.2, and pH = 7.4. PMN intracellular pH was measured spectrofluorometrically. Leukocyte CD11b, CD18 and CD14 were measured by flow cytometry using monoclonal antibodies in otherwise unstimulated cells or 60 minutes after lipopolysaccharide (LPS) stimulation. In addition, leukocyte adhering capacity to nylon wool was tested. In an attempt to dissect the effect of high glucose concentrations from that of the attendant hyperosmolality, the experiments were repeated with dialysates in which glucose was substituted by sodium chloride (NaCl-PDS) to attain identical osmolalities. G-PDS, as well as the mixtures of spent and fresh G-PDS, significantly depressed the basal PMN expression of adhesion receptors CD11b and CD18 and monocyte expression of CD14, and substantially mitigated the LPS-mediated up-regulation of CD11b and CD18. Likewise, G-PDS significantly inhibited leukocyte adhering capacity without affecting cell viability. Similar results were observed with NaCl-PDS. The observed abnormalities were primarily osmolality-dependent, and largely intra- and extracellular pH-independent. Impaired adhesion receptor expression and cell adhesion capacity shown here reveal another dimension of the G-PDS-induced leukocyte abnormalities.
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PMID:Effects of conventional peritoneal dialysates on leukocyte adhesion and CD11b, CD18 and CD14 expression. 891 36

Hemoglobin (Hb) is a toxic molecule responsible for the extreme lethality associated with experimental Escherichia coli peritonitis, but the mechanism has yet to be elucidated. Hb, but not globin, showed toxic effects in a live E. coli model but not in a model using killed E. coli. Methemoglobin, hematin, and the well-known Fenton reagents iron and iron-EDTA demonstrated the same lethal effect in E. coli peritonitis as Hb, while the addition of the Fenton inhibitors desferrioxamine (DF) and diethylenetriamine pentaacetate removed most of the cytotoxic activity of iron. Administration of a combined dose of superoxide dismutase and catalase minimized the action of Hb and iron-EDTA, suggesting that both O(2)(.-) and H(2)O(2) are involved in the toxic action of Hb in this rat model. The combination of the antioxidative enzymes and DF further suppressed iron-mediated lethality. An electron spin resonance technique with the spin-trapping reagent 5, 5-dimethyl-1-pyroline-N-oxide (DMPO) showed O(2)(.-) generation in the peritoneal fluid of rats injected with E. coli alone or E. coli plus iron-DF, and (.)OH generation was detected in the peritoneal fluid of the rats injected with iron-EDTA. Hb did not show any spin adduct of oxygen radicals, suggesting that Hb produces non-spin-trapping radical ferryl ion, which decayed the spin adduct of DMPO. In the presence of Hb or iron-EDTA, O(2)(-)-generating activity and viability of phagocytes decreased, whereas lipid peroxidation of peritoneal phagocytes increased. Generation of oxygen radicals and lipid peroxidation did not differ in the live and dead bacterial models. Bacterial numbers in the peritoneal cavity and blood were markedly increased in the live bacterial model with Hb and iron-EDTA. The Fenton inhibitor iron-DF prevented the loss of phagocyte function, lipid peroxidation, and bacterial proliferation. These results led us to conclude that the lethal toxicity of Hb in bacterial peritonitis is associated with a Fenton-type reaction, the products of which decrease phagocyte viability, through the induction of lipid peroxidation, allowing bacterial proliferation and resulting in mortality.
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PMID:Hemoglobin toxicity in experimental bacterial peritonitis is due to production of reactive oxygen species. 1054 90

Cirrhosis is associated with altered gastrointestinal function, and bacterial translocation from the gut plays an important role in the etiology of spontaneous bacterial peritonitis (SBP) seen in this condition. Although alterations in gut motility and intestinal permeability are recognized in cirrhosis, the intestinal damage at the cellular and subcellular levels is not well understood. This study looked at the mucosal alterations in experimental cirrhosis and the role of oxygen free radicals in this process. It was shown that cirrhosis results in oxidative stress in the intestine, as seen by increased xanthine oxidase (XO) activity and altered antioxidant status. Cirrhosis also affects enterocyte mitochondrial function, as assessed by respiratory control ratio, swelling, and calcium flux. Increased lipid peroxidation of the brush border membranes (BBMs) was seen along with altered intestinal transport. In conclusion, this study shows that intestinal mucosal alterations are seen in experimental cirrhosis and are possibly mediated by oxidative stress.
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PMID:Intestinal mucosal alterations in experimental cirrhosis in the rat: role of oxygen free radicals. 1187 Mar 76

TLRs are considered important for the control of immune responses during endotoxic shock or polymicrobial sepsis. Signaling by TLRs may proceed through the adapter proteins MyD88 or TIR domain-containing adaptor inducinng IFN-beta. Both pathways can lead to the production of type I IFNs (IFN-alphabeta). In the present study, the role of the type I IFN pathway for host defense and immune pathology in sepsis was investigated using a model of mixed bacterial peritonitis. Systemic levels of IFN-alphabeta protein were markedly elevated during septic peritonitis. More detailed analyses revealed production of IFN-beta, but not IFN-alpha subtypes, and identified CD11b+ CD11c- macrophage-like cells as major producers of IFN-beta. The results further demonstrate that in IFN-alphabeta receptor I chain (IFNARI)-deficient mice, the early recruitment of neutrophils to the infected peritoneal cavity was augmented, most likely due to an increased local production of MCP-1 and leukotriene B4. In the absence of IFNARI, peritoneal neutrophils also exhibited enhanced production of reactive oxygen intermediates and elevated expression of Mac-1. Conversely, administration of recombinant IFN-beta resulted in reduced leukotriene B4 levels and decreased peritoneal neutrophil recruitment and activation. Analysis of the cytokine response to septic peritonitis revealed that IFNARI deficiency strongly attenuated late, but not early, hyperinflammation. In accordance with these findings, bacterial clearance and overall survival of IFNARI(-/-) mice were improved. Therefore, the present study reveals critical functions of the type I IFN pathway during severe mixed bacterial infections leading to sepsis. The results suggest that type I IFN exerts predominantly adverse effects under these conditions.
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PMID:Type I IFN modulates host defense and late hyperinflammation in septic peritonitis. 1701 50

We have reported that an extract of the edible officinal mushroom Agaricus blazei Murill (AbM) stimulates synthesis of pro-inflammatory cytokines in human monocytes and vein endothelial cells in vitro and reduces the extent of lethal septicemia in mice with bacterial peritonitis. In the present study on human monocytes and granulocytes in whole blood ex vivo, we studied the dynamic changes of cell adhesion molecules (CD11b, CD62L) and the production of reactive oxygen species (ROS) after stimulation with AbM. The presence of AbM resulted in a similarly increased expression of CD11b in monocytes and granulocytes, although at a lower AbM concentration in monocytes (0.5%) than in granulocytes (2%). Furthermore, there was an AbM-mediated decrease in CD62L expression mirroring the effect on CD11b expression regarding magnitude and dose response. The intracellular production of ROS increased slightly but significantly in granulocytes, but not in monocytes stimulated with AbM. The results suggested that the major effect of AbM on monocytes and granulocytes was the upregulation of CD11b expression, thereby increasing both the phagocytic potential and the ablility to induce diapedesis into inflammatory foci. The rich beta-glucan content of AbM could play a crucial role in this immune response.
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PMID:Effect of an extract of the mushroom Agaricus blazei Murill on expression of adhesion molecules and production of reactive oxygen species in monocytes and granulocytes in human whole blood ex vivo. 1755 Mar 80

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