UMLS:C0031154 - FACTA Search

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Query: UMLS:C0031154 (peritonitis)
15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An in vivo experimental peritonitis model was investigated in the rabbit using zymosan as the inflammatory stimulus. After an i.p. injection of zymosan, exudate was removed at intervals and tested in the back skin of assay rabbits. Assay rabbits received i.v. injections of 125I-albumin and 111In-neutrophils, and the local accumulation of each label was measured in response to intradermal injections of exudate samples mixed with a potentiating dose of PGE2. When peritoneal exudate samples were tested in the presence of a specific anti-C5a antibody, virtually all the edema-inducing and neutrophil chemoattractant activity was abolished in samples taken up to 2 h after the zymosan injection. Later samples, however, contained increasing levels of a non-C5a component. In C5a-depleted 6-h exudate two peaks of inflammatory activity were separated using cation exchange HPLC. Evidence is presented that C5a itself is unable to stimulate the production of these activities. Both peaks of activity appear related to IL-8/NAP-1 as they inhibited the binding of 125I-IL-8/NAP-1 to human neutrophils.
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PMID:The sequential generation of neutrophil chemoattractant proteins in acute inflammation in the rabbit in vivo. Relationship between C5a and proteins with the characteristics of IL-8/neutrophil-activating protein 1. 189 60

A total of 105 patients participated in this study, including 10 with chronic glomerulonephritis with normal renal function (CGN patients), 36 uraemic patients (CRF patients), 19 continuous ambulatory peritoneal dialysis patients (CAPD) without peritonitis, three CAPD patients with peritonitis, 37 patients undergoing chronic haemodialysis (HD) divided into short-term HD, 15 patients; medium-term HD, 12 patients; and long-term HD, 10 patients. IL-8 and two other proinflammatory cytokines, IL-6 and TNF alpha were tested using a specific immunoassay. IL-8, IL-6, and TNF alpha serum levels were significantly increased in patients with chronic renal failure compared to their levels in normal individuals (P < 0.0001, P < 0.05 and P < 0.0001 respectively). The most pronounced increment in IL-8, IL-6 and TNF alpha serum levels was observed in CAPD patients (P < 0.0001). CAPD patients without peritonitis showed relatively low levels of IL-8 or IL-6 in peritoneal dialysate effluents (PDE), whereas PDE-TNF alpha were not detectable in almost all patients tested. Patients with peritonitis showed very high serum and PDE levels of IL-8, IL-6 and TNF alpha. The clinical recovery from peritonitis was characterized by a rapid fall in IL-8, IL-6 and TNF alpha in serum and dialysate. HD patients showed a significant increase in serum levels of IL-8 and also IL-6 and TNF alpha compared to normal individuals (P < 0.05, P < 0.05 and P < 0.01 respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interleukin-8 in chronic renal failure and dialysis patients. 781 57

Interleukin-8 (IL-8) has been reported to be released by activated peritoneal macrophages (PMs) and a variety of other cell types, and it exhibits potent chemotactic activity for polymorphonuclear cells (PMNs). We have previously shown that IL-8 is detectable in the drain dialysate of uremic patients on continuous ambulatory peritoneal dialysis (CAPD) during peritonitis. The levels of IL-8 in infected drain dialysate caused by different microorganisms were variable. In this study, we evaluated the gene expression and release of IL-8 by PMs and PMNs during peritonitis caused by Staphylococcus aureus in uremic patients on CAPD. IL-8 levels were variable in the drain dialysate at the different episodes of peritonitis, even in the same patient. The IL-8 levels were highly correlated with PMN count in drain dialysate (r = 0.9919, p < 0.001). PMs and PMNs obtained from drain dialysate at the onset of peritonitis increased mRNA expression for IL-8 and the amount of IL-8 mRNA from drainage cells was also highly correlated with PMN count. In contrast, cells isolated from drain dialysate without peritonitis failed to express mRNA for IL-8. These data suggest that increased expression of IL-8 may be a feature of peritonitis. The levels of IL-8 during peritonitis were not only related to the etiological microorganism but also to other unknown factor(s).
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PMID:Gene expression and release of interleukin-8 by peritoneal macrophages and polymorphonuclear leukocytes during peritonitis in uremic patients on continuous ambulatory peritoneal dialysis. 787 Feb 28

To examine RNA/protein synthesis of neutrophils and related dynamic changes during the inflammatory process, we investigated mRNA expressions in neutrophils, by RNA blot hybridization analyses using 12 different rabbit gene probes. We first selected five candidate genes encoding inflammation-related proteins, i.e. tumor necrosis factor (TNF-alpha) IL-1 alpha, IL-1 beta, neutrophil activating peptide-1/IL-8 (NAP-1/IL-8) and monocyte chemoattractant protein (MCP)-1. We further selected several genes on basis of the results from gene subtraction between cDNA libraries from neutrophils at an early (5 h) and at a late (24 h) stage of casein-induced acute peritonitis in rabbits, i.e. immune activation gene-2 (Act-2), migration inhibitory factor-related protein-8 (MRP-8), MRP-14, gamma-actin, and formyl-methionyl-leucyl-phenylalanine receptor (fMLP-R), and ferritin light (L) chain. In addition to these genes we used ferritin heavy (H) chain gene, another component of the ferritin molecule. We examined mRNA expressions by cytoplasmic slot blot analysis of the above 12 genes in neutrophils obtained from blood and from various stages of casein-induced inflammation in rabbits. The observed patterns of mRNA expression kinetics were classified into three. Pattern 1: mRNAs of MRP-8, MRP-14, and gamma-actin were constitutively expressed in blood neutrophils, and increased rapidly after emigration into inflammatory sites. Pattern 2: mRNAs of IL-1 beta, NAP-1/IL-8, Act-2, and fMLP-R were undetectable in blood neutrophils, and were induced rapidly after the onset of inflammation. Pattern 3 mRNAs of ferritin L and H chain were induced slowly, and increased with progression of the inflammatory process.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dynamic changes in mRNA expression of neutrophils during the course of acute inflammation in rabbits. 814 23

We investigated interleukin-6 (IL-6) and interleukin-8 (IL-8) in peritoneal dialysate and serum from 17 patients on continuous ambulatory peritoneal dialysis (CAPD) with a total of 24 episodes of peritonitis and from 14 non-infected CAPD controls. Bacterial growth was found in 20 (83%) of the dialysate samples. Staphylococcus epidermidis caused 40% of the culture-verified peritonitis. Samples from dialysate were obtained during the first month of dialysis and during peritonitis from the first three dialysate bags on day 1 (the day of admittance) and from night bags on days 3 and 10. Serum samples were drawn on days 1 and 10. Interleukin-6 was increased in all dialysate samples on day 1. The peak median concentration was 23,500 pg/mL (range 1,710 to 340,000 pg/mL) in the first dialysate. Interleukin-8 was also elevated from all patients in the first dialysate, with a peak median value of 2,000 pg/mL (range, 110 to 185,000 pg/mL). Interleukin-6 and IL-8 concentrations from peritoneal fluid on days 1, 3, and 10 were significantly higher than concentrations from CAPD controls (IL-6 median value, 90 pg/mL, P < 0.001; IL-8 median value, nondetectable, P < 0.001). In serum, IL-6 and IL-8 were detected in 83% and 65% of the episodes, respectively. A correlation (P = 0.007) was seen between IL-6 and IL-8 in the first dialysate sample, but not in the subsequent dialysate samples. The highest acute phase reactant (CRP) level obtained during the peritonitis episode correlated to IL-6 in serum (P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interleukin-6 and interleukin-8 in dialysate and serum from patients on continuous ambulatory peritoneal dialysis. 837 40

The activity of the steroid-inducible protein lipocortin-1 (LC1; with a primary sequence of 346 amino acids; also called annexin 1), a fragment corresponding to amino acids 1-188 and a short peptide from the N-terminus (amino acid 2-26) were tested for anti-inflammatory actions in three models of acute inflammation in the mouse in comparison with a mAb anti-CD11b (alpha CD11b). In the mouse air-pouch model LC1, fragment 1-188 and peptide Ac2-26 exhibited powerful inhibitory effects (ED50 approximately 5.2, 38 and 88 micrograms/mouse, respectively) on leukocyte migration elicited by IL-1. LC1 was approximately 200 times more potent than Ac2-26 on a molar basis although both gave maximal inhibitions, in contrast fragment 1-188 only produced a partial dose-response curve. LC1 was approximately 20 times more potent on a molar basis in this assay than the alpha CD11b mAb. Peptide Ac2-26 and the mAb alpha CD11b also blocked cell migration into the air-pouch induced by IL-8 with approximately the same potency. In the mouse skin edema and zymosan peritonitis assays Ac2-26 was inhibitory (ED50 of 200 micrograms/mouse) but less so than the alpha CD11b antibody (ED50 approximately 0.5 mg/mouse). Both LC1 (10 micrograms) and Ac2-26 (200 micrograms) completely blocked FMLP-induced neutropenia in the mouse. Studies using an inactivated LC1 preparation, which binds to the same high affinity binding sites as the biologically active material, indicated that the short peptide acts on the same sites as the native LC1. This study confirms the activity of LC1 in another model of experimental inflammation and suggests that it acts partly through inhibition of leukocyte activation with an overall effect qualitatively comparable to the blocking of CD11b portion of a beta 2-integrin complex. It also shows that peptides derived from the N-terminal domain of LC1 may mimic the activity of the full length molecule and points the way for a new family of anti-inflammatory substances that inhibit leukocyte trafficking.
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PMID:Lipocortin-1 fragments inhibit neutrophil accumulation and neutrophil-dependent edema in the mouse. A qualitative comparison with an anti-CD11b monoclonal antibody. 840 3

In this study, we investigated whether peritoneal dialysate interleukin-6 (IL-6) and IL-8 levels were elevated during peritonitis in continuous ambulatory peritoneal dialysis (CAPD) patients, with special reference to the high peritonitis occurrence (HPO) group. Serial measurements of IL-6 and IL-8 levels in dialysate before, during and after resolution of peritonitis were done in 13 CAPD patients with 15 episodes of peritonitis. Based on the peritonitis occurrence, 7 patients were assigned to the low peritonitis occurrence (LPO) and 6 patients to the HPO group. Marked elevation of IL-6 and IL-8 in drain dialysate occurred in the early period of peritonitis especially on the first 2 days in both groups. However, there were no significant differences between the groups in the levels of IL-6 and IL-8 in drain dialysate on the first day of peritonitis. However, the disappearance of peritoneal dialysate IL-8 level was faster in the LPO than in the HPO group. The decrease in IL-8 levels during peritonitis was faster than that of IL-6. Marked elevation of IL-6 and IL-8 in drain dialysate was found in the patient with peritonitis caused by Staphylococcus epidermidis and mixed gram-negative bacilli. Therefore, we hypothesize that when peritonitis occurs too frequently in a short period in the HPO group, more IL-6 and IL-8 have been produced in the peritoneum contributing to the ongoing peritoneal injury and/or fibrosis.
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PMID:Serial changes of interleukin-6 and interleukin-8 levels in drain dialysate of uremic patients with continuous ambulatory peritoneal dialysis during peritonitis. 845 75

The migration of leukocytes, including polymorphonuclear neutrophils and monocytes, into the peritoneal cavity is a key event of intraperitoneal inflammation. We investigated the levels of two members of the chemokine family, interleukin 8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1), in the dialysate effluent of 18 continuous ambulatory peritoneal dialysis (CAPD) patients with peritonitis and compared them with chemokine levels in noninfected CAPD effluent. Being a major source of inflammatory cytokines, we also isolated peritoneal macrophages from peritonitis effluent to determine the mRNA expression directly after isolation. The mean (SEM) concentrations of IL-8 and MCP-1 were significantly higher in the effluent of peritonitis patients than in noninfected effluents MCP-1: 22.5 +/- (6.27) versus 0.37 +/- (0.1) ng/mL and IL-8: 2.39 +/- (1.15) versus 0.04 +/- (0.01) ng/mL. Northern blot analysis of isolated effluent macrophages revealed strong signals for MCP-1 and IL-8. Our findings showed that CAPD effluent from patients with peritonitis contains markedly elevated MCP-1 and IL-8 levels, suggesting that these chemokines participate in leukocyte recruitment during CAPD peritonitis. Isolation of mRNA of peritonitis-derived peritoneal macrophages revealed strong signals for MCP-1 and IL-8, suggesting that macrophages are a major source of these inflammatory mediators.
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PMID:MCP-1 levels are elevated in peritonitis fluid from CAPD patients due to secretion by peritoneal macrophages. 853 2

Dialysate and serum levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and IL-1-ra were investigated in 20 patients on continuous ambulatory peritoneal dialysis (CAPD), who altogether had 30 episodes of peritonitis. Bacterial growth was found in 25 (83%) of the dialysate samples. Staphylococcus epidermidis was the single most common microorganism, found in 44% of the culture-verified peritonitis. Samples from dialysate bags were obtained during the first month of dialysis and during peritonitis from the first three bags on day 1 (the day of admittance) and from night bags on days 3 and 10. Serum samples were drawn on days 1 and 10. The peak concentrations of cytokines occurred on the first day of infection. In dialysates, TNF-alpha was elevated in 96% of the patients, with a peak median concentration of 160 pg/mL (range, <15 to 4,400 pg/mL). Seventy-five percent of the dialysates had elevated IL-1-beta, with the highest median level of 52 pg/mL (range, <10 to 940 pg/mL), whereas all patients had elevated IL-1 ra, with a peak median value of 10,300 pg/mL (range, 470 to 79,000 pg/mL). TNF-alpha, IL-1 beta, and IL-Ira were significantly higher than in corresponding noninfected samples (TNF-alpha median value, <15 pg/mL; IL-1 beta, <10 pg/mL; and IL-1-ra, 150 pg/mL; P < 0.0001, P < 0.002, and P < 0.001, respectively). In serum, elevated TNF-alpha levels were found in 92% of the episodes, but the median levels were less than one third of the corresponding lavage levels. IL-1-beta was detected in 8% of the episodes and, although IL-1-ra was found in 92% of the patients, the dialysate levels were more than 15 times higher. In dialysate, a correlation was observed for TNF-alpha and IL-Ira and also between IL-1-beta and IL-Ira. IL-1 beta and IL-1-ra also correlated with the previously analyzed IL-6, and IL-1-beta correlated with the previously analyzed IL-8. Patients infected with high virulent strains had higher cytokine levels as compared with those infected with low virulent strains. In conclusion, our study shows markedly elevated TNF-alpha, IL-1 beta, and IL-1-ra levels in the acute stage in CAPD patients with peritonitis.
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PMID:Tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-1 receptor antagonist in dialysate and serum from patients on continuous ambulatory peritoneal dialysis. 860 10

Our objective was to determine the incidence of peritonitis episodes with an impaired initial cell reaction (IICR:neutrophil number < 100 x 10(6)/L) over a period of ten years, and to find possible explanations for this unusual presentation of peritonitis. A retrospective review of the files of continuous ambulatory peritoneal dialysis (CAPD) patients included in the CAPD program 1984 and 1993 was done. Analysis of cytokine and prostanoid patterns during four peritonitis episodes with an IICR was compared to 12 episodes with a normal initial cell reaction (NICR). Dialysate cell numbers and immunoeffector characteristics of peritoneal cells were compared in 7 IICR patients in a stable situation and a control group of 70 stable CAPD patients. The setting was a CAPD unit in the Academic Medical Center in Amsterdam. Thirty-five CAPD patients who had one or more peritonitis episodes with an IICR and a control group of 249 CAPD patients were included in the study. The incidence of peritonitis with an IICR was 6%. These episodes occurred more than once in 51% of the patients who presented with IICR. In 72% the cell reaction was only delayed: a cell number exceeding 100 x 10(6)/L was reached later. Staphylococcus aureus was significantly more frequently the causative microorganism compared to all peritonitis episodes (PE) that occurred during the study period. Patients with IICR had lower dialysate cell counts in a stable situation, compared to a control group (p < 0.01). This was caused by a lower number of macrophages and CD4 positive lymphocytes. The phagocytosis capacity of the macrophages appeared to be normal. In a comparison of four PE with an IICR and 12 episodes with an NICR, the tumor necrosis factor-alpha (TNF-alpha) response was similar and occurred on day 1, also pointing to normally functioning macrophages. However, the maximal appearance rates of interleukin-6 (IL-6) and IL-8 occurred later in the episodes with IICR compared to NICR (day 2 vs day 1, p < 0.05). No differences were found in vasodilating prostaglandins, mesothelial cell markers (cancer antigen 125, phospholipids, hyaluronan), and mesothelial cell numbers in the stable situation nor during peritonitis. Peritonitis can present as abdominal pain in the absence of a cloudy dialysate. In some of the patients this presentation occurred more than once. This impaired, most often delayed, cell reaction was associated with a delayed secondary cytokine response. As IL-6 and IL-8 can be synthesized by mesothelial cells, this suggests an impaired functioning mesothelium. This could not be confirmed, however, by a lower number of mesothelial cells in effluent or lower dialysate levels of mesothelial cell markers.
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PMID:Impaired initial cell reaction in CAPD-related peritonitis. 872 24

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