Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031154 (peritonitis)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although 58 patients with peritonitis carcinomatosa underwent multidisciplinary therapy over the last 5 years in our department, about half of them died within 3 months after treatment. In addition, the prognosis was poor for gastric and colon cancer patients, who had macroscopic peritoneal dissemination. Therefore intraoperative intraperitoneal administration of either BRM or anticancer drugs was performed for the microscopic peritoneal dissemination of the cancer, and the immunological response in the peritoneal cavity was examined. In terms of subpopulation of peritoneal exudate cells, neutrophil leucocytes were predominant and thereafter lymphocytes increased. As for the cytokines in the exudate from peritoneal cavity, the concentration of interleukin-6 peaked within 24 hours after administration, followed by a gradual decrease, while the concentration of interferon-gamma was detectable at more than 24 hours after operation, followed by a gradual increase. Tumor necrosis factor-alpha was also detectable in the exudate. Its concentration decreased when both OK-432 and MMC were administered, but it increased when CDDP was administered. The above results indicated that preventive intraoperative intraperitoneal administration of BRM and anticancer drugs should bring about individual immunokinetic modulation in tumor bearing host and both cytokines and immunocytes could play an important role in locoregional tumor immunity.
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PMID:[Clinical studies on locoregional immunochemotherapy of peritonitis carcinomatosa]. 153 Mar 41

The development of useful therapy for the peritonitis carcinomatosa of gastrointestinal cancer is an important theme in cancer therapy. We developed an experimental model of peritonitis carcinomatosa in nude mice transplanted intraperitoneally human colon cancer cells. In this study, we investigated combined effect of human recombinant interferon-beta (rIFN-beta) and recombinant interferon-gamma (rIFN-gamma) in vivo using this model. The result indicate that each rIFN-beta and rIFN-gamma showed a significant prolonged survival compared with the control group (mean survival days: 41.8 +/- 5.0 days). Furthermore, combined administration of rIFN-beta and rIFN-gamma showed a marked prolonged survival (mean survival days: 114.0 +/- 7.4 days) compared with rIFN-beta or rIFN-gamma alone. These results suggest that a combined treatment of rIFN-beta and rIFN-gamma may be useful against peritonitis carcinomatosa of gastrointestinal cancer.
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PMID:[Combined effect of human recombinant interferon-beta and interferon-gamma against an experimental model of peritonitis carcinomatosa in nude mice]. 310 28

Peritoneal cells were isolated from dialysates drained from nine patients on continuous ambulatory peritoneal dialysis (CAPD) during episodes of peritonitis. Levels of expression of mRNA for the regulatory cytokines, interferon-gamma (IFN-gamma) and IL-4, were investigated daily, where possible, during the first 5 days of peritonitis. Cytokine mRNA levels were compared with those of peripheral blood mononuclear cells (PBMC) stimulated in vitro with phorbol 12-myristate 13-acetate (PMA) plus phytohaemagglutinin (PHA). Peritoneal cells expressed low levels of IFN-gamma mRNA; for four of nine patients, IL-4 mRNA levels greater than those expressed by stimulated PBMC were detected. There was no pattern of cytokine mRNA expression associated with the types of organisms detected in dialysates at initiation of peritonitis. However, in contrast to those patients with a transient, resolving peritonitis, significant IL-4 mRNA expression was detected in cells isolated early in the episodes of peritonitis in patients who suffered recurrent peritonitis within 30 days of the initial peritonitis episode. These results suggest an association between early IL-4 mRNA expression and susceptibility to further infections. The known anti-inflammatory effects of IL-4 may explain this association.
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PMID:IL-4 mRNA expression by peritoneal cells during episodes of peritonitis in patients on continuous ambulatory peritoneal dialysis. 774 64

Strains of Staphylococcus aureus, isolated from the effluent of patients with peritonitis on CAPD (continuous ambulatory peritoneal dialysis), adhered well to both cultured human mesothelial cells and to fibronectin, but not to laminin or gelatin. Mesothelial cells grown in medium M199 exhibited more surface fibronectin compared to cells grown in MEM-Dval and demonstrated higher levels of S. aureus adherence. Soluble fibronectin concentrations up to 10 micrograms/ml increased the adherence of S. aureus to cultured mesothelial cells. The dose-response curve was consistent with the binding of fibronectin to a saturable receptor of apparent dissociation constant (KD) = 1.7 x 10(-10) M. This corresponds closely to the KD (2 x 10(-10) M) of the staphylococcal fibronectin-binding protein. S. aureus adherence was increased following the preincubation of mesothelial cell monolayers with interleukin-1 and was maximal after 6 h preincubation. Treating mesothelial cells with interferon-gamma for 48-72 h reduced the adherence of S. aureus.
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PMID:Adherence of Staphylococcus aureus to cultures of human peritoneal mesothelial cells. 838 38

Interferon-gamma, a cytokine, is produced by lymphocytes when they are stimulated by cytokines from activated macrophages, and is essential for macrophage-mediated bactericidal operations. To investigate whether a strain of bacteria can activate macrophages and lymphocytes, the interferon-gamma levels may thus be measured. Current literature maintains that peritoneal dialysis patients with recurrent peritonitis have "unhealthy" macrophages and lymphocytes unable to produce interferon-gamma, but that the administration of interferon improves the rates of peritonitis. In an in vitro experiment, Staphylococcus epidermidis, in both its planktonic and biofilm forms, was added to a suspension of peritoneal dialysis effluents, macrophages, and healthy peripheral blood lymphocytes, which were incubated at 37 degrees C for 18 h and then centrifuged. Subsequent levels of interferon-gamma were measured in the supernatants. Three such experiments were done with peritoneal macrophages and dialysis effluents collected from each of the three different patients involved in the study. It was found that little or no interferon-gamma (0.42 +/- 0.17 U/mL) was produced when biofilm bacteria were tested, but significant amounts of interferon-gamma (9.25 +/- 4.63 U/mL) resulted in conjunction with the planktonic form of the same bacteria. To eliminate experimental errors, all conditions were left identical, appropriate control groups were added, and each of the three experiments was duplicated. These in vitro data therefore provide new insight in the role of biofilm in the pathogenesis of recurrent peritonitis in peritoneal dialysis patients. Further clinical studies are required.
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PMID:Biofilm causes decreased production of interferon-gamma. 879 96

Mesothelial cells are actively involved in inflammatory processes by expressing a set of cell adhesion molecules (CAMs). Transmigration of leukocytes into inflamed tissues requires a chemotactic stimulus and engagement of platelet-endothelial cell adhesion molecule-1 (PECAM-1). To investigate the kinetics involved in peritonitis, pure cultures of mesothelial cells are necessary. In previous studies, we have found that human mesothelial cells (HOMES) show a weak constitutive expression of PECAM-1, which cannot be further stimulated by cytokines. It is known that all serous cavities and body fluids contain numerous macrophages which strongly express this adhesion molecule. To identify the cells responsible for the expression of PECAM-1, mesothelial cells freshly obtained from omental tissue were isolated using PECAM-1-conjugated magnetic beads by cell sorting. For these studies, the negative as well as the positive fraction of isolated cells were used. As a control, freshly isolated monocytes were studied. Cell cultures were characterized by light and electron microscopy, as well as immunocytochemistry. The negative cell fraction was cultivated and stimulated for different times with tumor necrosis factor-alpha (30 and 300 U/ml), interleukin-1 beta (10 and 100 U/ml) and interferon-gamma (500 U/ml) and PECAM-1 expression was analyzed by a comparative quantitative cell enzyme immunoassay (EIA). The positive cell fraction was treated in the same manner. Both fractions of isolated cells showed strong positivity for cytokeratins 8, 18, 7 and 19, as well as vimentin. CD68, a monocyte marker, was not detected on mesothelial cells. In addition, EIA analysis confirmed the constitutive expression of PECAM-1 obtained from previous studies. This expression on HOMES was not inducible, irrespective of the type and concentration of cytokine studied. These data confirm PECAM-1 expression on mesothelial cells obtained from human omental tissue and suggest a critical role in transmigration of leukocytes during peritoneal inflammation.
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PMID:PECAM-1 expression in human mesothelial cells: an in vitro study. 915 26

Recent studies have emphasized the role of peritoneal mesothelial cell (PMC) in peritoneal immune defense mechanisms in continuous ambulatory peritoneal dialysis (CAPD). The aim of this study was to evaluate a possible relationship between peritoneal dialysis effluent (PDE), cytokine (Cy) levels, and PMC viability and their impact on peritonitis morbidity. Fifteen patients initiating CAPD for end-stage renal failure participated in the study. The following parameters were evaluated: (1) the levels of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-6 (IL-6), and interleukin-8 (IL-8) in PDE samples taken 7 days after initiating CAPD, at the end of the first, third, and sixth month of CAPD (determined by a solid phase enzyme amplified sensitivity immunoassay EASIA); (2) peritoneal mesothelial cell viability [determined by the release of lactate dehydrogenase (LDH) and by trypan blue extrusion test] by isolating and culturing peritoneal mesothelial cells at the moment of the placement of the peritoneal catheter and at the sixth month of CAPD; (3) peritonitis incidence during the 24 months after starting CAPD. At the first month of CAPD in all patients there was a slight increase in PDE IL-1 beta and TNF-alpha levels, while other Cy were almost undetectable. Time course studies showed that in 10 patients (Group I) there was a significant increase in PDE levels of IL-6, IL-8, and INF-gamma (p < 0.0005) in comparison to other Cy and a good PMC viability. In the other 5 patients (Group II) there were higher PDE levels of IL-1 beta and TNF-alpha (p < 0.0005). This was associated with a marked reduction in PMC viability determined by the release of LDH and by the trypan blue extrusion test. During the 24 months after starting CAPD, incidence of peritonitis was one episode per 24 patient-months in Group I and one episode per 9.2 patient-months in Group II. Our results show that from the beginning of CAPD there are distinct patterns of Cy in the PDE that correlate with a different PMC viability and peritonitis morbidity. Thus the analysis of the above-mentioned parameters may be useful in the early identification of the risk of peritonitis, thus allowing preventive measures.
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PMID:Peritoneal dialysis effluent, cytokine levels, and peritoneal mesothelial cell viability in CAPD: a possible relationship. 936 Jun 42

Overproduction of nitric oxide (NO) upon expression of inducible NO synthase (iNOS) may be responsible for refractory hypotension in septic shock. Whereas high levels of NOS activity have been documented in experimental models of endotoxemia or intravenous challenge with Escherichia coil, much less is known concerning tissue models of Gram-negative infection. We examined NO production (measured as the accumulation of plasma NO3- + NO2-) in a murine model of Gram-negative peritonitis. Plasma NO3- + NO2- increased progressively from 25 microM to peak levels of 50-150 microM 24 h after intraperitoneal challenge with E. coli 0111:B4, similar to values reported for septic shock patients. Treatment of infected mice with NG-monomethyl-L-arginine, an inhibitor of NOS activity, resulted in the efficient inhibition of NO3- + NO2- production. In order to evaluate the roles of interferon-gamma (IFN-gamma) and tumor necrosis factor (TNF-alpha) in the induction of NO synthesis in murine peritonitis, mice deficient in the respective cytokine receptors were studied. In control in vitro experiments, macrophages from IFN-gammaR- or TNFR55-deficient mice, while failing to respond to IFN-gamma or TNF-alpha, respectively, produced high levels of NO under appropriate stimulation. When challenged intraperitoneally with E. coli, IFN-gammaR- or TNFR55-deficient mice exhibited similar levels of bacteremia and NO production as their wild-type controls. These data thus suggest that enhanced NO production during focal Gram-negative infection may occur in the absence of signaling through either IFN-gammaR or TNFR55.
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PMID:Nitric oxide production in experimental gram-negative infection: studies with cytokine receptor-deficient mice. 968 89

Peritoneal mesothelial cells are uniquely located to regulate cellular events in the peritoneal cavity and are an important source for various cytokines and growth factors. This study was conducted to analyze the capacity of human peritoneal mesothelial cells (HPMCs) to synthesize and release basic fibroblast growth factor (bFGF) and to characterize its regulation by inflammatory cytokines. HPMCs constitutively synthesized and released considerable amounts of bFGF as detected by a specific immunoassay. Almost 80% of bFGF (1547 +/- 173 pg/10(5) cells) was localized intracellularly. Approximately 20% of the bFGF (357 +/- 27 pg/10(5) cells) was associated with extracellular matrix components on the HPMC surface. Small amounts of bFGF (<1%) were detectable in tissue culture supernatants (8.4 +/- 1.4 pg/10(5) cells). Treatment of HPMCs with interleukin-1beta (IL-1beta; 1 ng/ml) resulted in a significant increase in bFGF production. The intracellular bFGF content showed a rapid but only transient increase, which was significant above background levels after 24 hours (41% increase; P < 0.05). This increase in intracellular bFGF concentration was associated with an induction of the release of bFGF. Within 96 hours, the release of bFGF to the cell surface and into the supernatant increased by 58% (564 +/- 52.4 pg/10(5) cells; P < 0.01) and by 214% (26.4 +/- 3.2 pg/10(5) cells; P < 0.001), respectively. Neither tumor necrosis factor-alpha nor interferon-gamma affected bFGF synthesis by HPMCs. Stimulation of HPMCs with IL-1beta increased steady-state levels of bFGF-specific mRNA. Immunohistochemical analyses of peritoneal tissue revealed constitutive expression of bFGF by HPMCs. This in situ expression proved to be most pronounced in areas of serosal inflammation in activated HPMCs. Our study demonstrates that HPMCs synthesize and release significant amounts of bFGF and that the expression of this growth factor is significantly up-regulated by the proinflammatory cytokine IL-1beta. The data support the view that HPMCs are key regulators of abdominal disease processes such as peritonitis, peritoneal fibrosis, or peritoneal tumor metastasis.
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PMID:Basic fibroblast growth factor synthesis by human peritoneal mesothelial cells: induction by interleukin-1. 1059 27

A model of lipoplex-induced peritonitis was used to characterize the inflammatory response to cationic lipid:DNA lipoplexes with respect to activation of host antitumoral effector mechanisms. Three different cationic lipids were used in these studies: N,N-dioleyl-N,N-dimethylammonium chloride (DODAC), N-(1-[2,3-dioleoyloxylpropyl)-N,N,N-trimethylammonium chloride (DOTAP), and N-(1-[2,3-dioleyloxy]propyl)-N,N,N-trimethylammonium chloride (DOTMA). The DODAC and DOTMA lipoplexes exhibited similar transfection properties in vitro, whereas the DOTAP lipoplexes transfected quite poorly in all cell lines tested. Intraperitoneal injection of cationic lipoplexes into immunocompetent mice resulted in a profound infiltration of inflammatory cells, secretion of interferon-gamma, and increased natural killer activity within the peritoneal cavity. Both DODAC and DOTMA lipoplexes produced similar inflammatory responses, lasting at least 5 days. The inflammation induced by DOTAP lipoplexes peaked by day 3 and resolved to near-control levels by day 5. These data indicate that although cationic lipid DNA complexes may differ in their inflammatory properties, the natural killer activation and interferon-gamma secretion that follow lipoplex administration should provide a functional adjuvant for cancer gene therapies that benefit from immunostimulation.
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PMID:Activation of host antitumoral responses by cationic lipid/DNA complexes. 1076 41


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