Value of scintigraphy in chronic peritoneal dialysis patients.
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BACKGROUND: A variety of factors can adversely impact chronic peritoneal dialysis (CPD) as an effective renal replacement therapy for patients with end-stage renal disease. These factors include peritonitis, poor clearances, loss of ultrafiltration, and a variety of anatomic problems, such as hernias, peritoneal fluid leaks, loculations, and catheter-related problems caused by omental blockage. This study reviews our experience with peritoneal scintigraphy for the evaluation of some of these difficulties. METHODS: From 1991 to 1996, 50 peritoneal scintigraphy scans were obtained in 48 CPD patients. Indications for scintigraphy were evaluated, and the patients were placed into four groups: group I, abdominal wall swelling; group II, inguinal or genital swelling; group III, pleural fluid; and group IV, poor drainage and/or poor ultrafiltration. A peritoneal scintigraphy protocol was established and the radiotracer isotope that was used was 2.0 mCi of 99mtechnetium sulfur colloid placed in two liters of 2.5% dextrose peritoneal dialysis solution. RESULTS: Ten scans were obtained to study abdominal wall swelling, with seven scans demonstrating leaks; six of these episodes improved with low-volume exchanges. Twenty scans were obtained to evaluate inguinal or genital swelling, and 10 of these had scintigraphic evidence for an inguinal hernia leak (9 of these were surgically corrected). One of four scans obtained to evaluate a pleural fluid collection demonstrated a peritoneal-pleural leak that corrected with a temporary discontinuation of CPD. Sixteen scans were obtained to assess poor drainage and/or ultrafiltration. Five of these scans demonstrated peritoneal location, and all of these patients required transfer to hemodialysis. The other 11 scans were normal; four patients underwent omentectomies, allowing three patients to continue with CPD. CONCLUSION: Peritoneal scintigraphy is useful in the evaluation and assessment of CPD patients who develop anatomical problems (such as anterior abdominal, pleural-peritoneal, inguinal, and genital leaks) and problems with ultrafiltration and/or drainage. (+info)
The requirement of an adherent cell substratum for the growth of developing plasmacytoma cells in vivo.
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The intraperitoneal injection of pristane (2,6,10,14-tetramethylpentadecane) produces an environment conductive to primary plasmacytoma growth in as few as 3 days. After pristane injection, the total free peritoneal cell population increases from a normal value of 1.55 X 10(6) to 5.28 X 10(6) and remains at this elevated level for at least 50 days. The adherent peritoneal cell population, composed of both mononuclear cells and polymorphonuclear leukocytes, is the primary source of this increase. In the pristane-conditioned peritoneum, these cells rapidly form a chronic granuloma on the peritoneal connective tissues. Daily subcutaneous treatment of mice with 0.5 mg of hydrocortisone beginning simultaneously with pristane injection prevents the increase in the peritoneal cell population, granuloma formation, d the production of a conditoned environment. In mice treated with hydrocortisone beginning 3 days after pristane injection, however, neither the peritoneal cell increase nor the production of a conditioned environment is prevented. The intraperitoneal injection of thioglycolate medium at 4-day intervals produces an elevation of the free adherent peritoneal cell population similar to pristane, but does not produce a granuloma or a conditioned environment. The intraperitoneal transfer of thioglycolate-induced adherent peritonel cells to mice treated with pristane and hydrocortisone simultaneously restores the production of a conditioned environment. These findings indicate that the adherent peritoneal cell population is responsible for the conditioning effect, and that the establishment of a resident population of these cells is necessary to produce conditioning. (+info)
LPS down-regulates the expression of chemokine receptor CCR2 in mice and abolishes macrophage infiltration in acute inflammation.
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Interactions between chemokines and their specific receptors are important for leukocyte trafficking. The CC-chemokine monocyte chemoattractant protein-1 (MCP-1) and its specific receptor CCR2 are essential in monocytic infiltration and have been associated with several inflammatory diseases. It has been reported that several endotoxin and proinflammatory cytokines inhibit CCR2 expression in vitro in human monocytes. We report here that lipopolysaccharides (LPS) down-regulated CCR2 expression both in vitro and in vivo. Injection of LPS into mice dramatically reduced the expression of CCR2 on the surface of peripheral blood cells and completely blocked macrophage infiltration into the peritoneal cavity in response to thioglycollate elicitation. In addition, treatment of mice with LPS reduced their efficiency to clear Listeria monocytogenes infection. These results suggest that down-regulation of CCR2 and blockage of monocyte infiltration may contribute to the inhibition of macrophage function in vivo by a low dose of LPS. (+info)
Disseminated tumor cells in pancreatic cancer patients detected by immunocytology: a new prognostic factor.
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Using an immunocytological approach, we previously showed that disseminated cancer cells are frequently found in peritoneal cavity and bone marrow samples of gastrointestinal and pancreatic cancer patients. Recently, we demonstrated that the detection of isolated tumor cells could serve as a new prognostic factor in gastric and colorectal cancer. Thus far, no conclusive data concerning the clinical implication of minimal residual disease in pancreatic cancer exist. In this study, we investigated peritoneal lavage and bone marrow samples of 80 pancreatic cancer patients to determine the predictive value of immunocytologically detected disseminated tumor cells. Therefore, immunocytological findings were correlated with the clinical follow-up data (median observation time, 10.7 months; range, 2-61 months), and the findings in peritoneal cavity and bone marrow samples were compared. Fifty-two % of the patients showed minimal residual disease at least in one compartment (39% positive lavage and 38% positive bone marrow samples). The detection rate of isolated tumor cells increased in parallel to the tumor stage. The presence of tumor cells in the peritoneal cavity significantly correlated with the survival time of the patients (P = 0.0035). In bone marrow samples, a strong trend was seen (P = 0.06). The evaluation of both compartments increased the number of positive patients and resulted in a highly significant correlation: all patients who were positive in at least one compartment died within 18 months, whereas negative patients showed a 5-year survival rate of 30% (P<0.0001). We recommend immunocytological investigation of peritoneal cavity and bone marrow samples as a new prognostic marker in pancreatic cancer patients. (+info)
CCAAT/enhancer binding protein epsilon is critical for effective neutrophil-mediated response to inflammatory challenge.
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Targeted mutation of CCAAT/enhancer binding protein (C/EBP) epsilon in mice results in early death, primarily due to spontaneous infection with Pseudomonas aeruginosa. Functional analysis of C/EBPepsilon-deficient neutrophils, in an in vivo model of peritoneal inflammation, shows multiple defects. Reduction of phagocytotic killing by C/EBPepsilon-deficient neutrophils is a result of decreased uptake of opsonized bacteria as well as little to no expression of secondary granule proteins. Abnormalities in neutrophil migration detected in a chemical peritonitis model are likely secondary to abnormal CD11b integrin and L-selectin expression on C/EBPepsilon-deficient neutrophils. Alterations in neutrophil cytokine expression in response to inflammation show decreased levels of interleukin-1 receptor antagonist (IL-1Ra) and increased levels of tumor necrosis factor-alpha (TNF-alpha) expression by C/EBPepsilon-deficient neutrophils. Additionally, TNF-alpha expression is increased in nonactivated, circulating C/EBPepsilon-deficient neutrophils. Overall, C/EBPepsilon-deficient neutrophils are severely functionally impaired, evoking an abnormal microenvironment, which may contribute to the loss of normal responses to inflammatory stimuli. Similarities between the C/EBPepsilon-deficient mouse model and the human disease, specific granule deficiency, will be discussed. (+info)
Different doses of adenoviral vector expressing IL-12 enhance or depress the immune response to a coadministered antigen: the role of nitric oxide.
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Joint immunization with two recombinant adenoviruses, one expressing hepatitis C virus (HCV) core and E1 proteins and another expressing IL-12 (RAdIL-12), strongly potentiates cellular immune response against HCV Ags in BALB/c mice when RAdIL-12 was used at doses of 1 x 105-1 x 107 plaque-forming units. However, cellular immunity against HCV Ags was abolished when higher doses (1 x 108 plaque-forming units) of RAdIL-12 were used. This immunosuppressive effect was associated with marked elevation of IFN-gamma and nitric oxide in the serum and increased cell apoptosis in the spleen. Administration of N-nitro-L -arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, to mice that received high doses of RAdIL-12 was lethal, whereas no apparent systemic toxicity by L -NAME was observed in those immunized with lower doses of the adenovirus. Interestingly, in mice immunized with recombinant adenovirus expressing core and E1 proteins of HCV in combination with RAdIL-12 at low doses (1 x 107 plaque-forming units), L -NAME inhibited T cell proliferation and CTL activity in response to HCV Ags and also production of Abs against adenoviral proteins. In conclusion, gene transfer of IL-12 can increase or abolish cell immunity against an Ag depending of the dose of the vector expressing the cytokine. IL-12 stimulates the synthesis of NO which is needed for the immunostimulating effects of IL-12, but apoptosis of T cells and immunosuppression ensues when IFN-gamma and NO are generated at very high concentrations. (+info)
Reciprocal effects of interleukin-4 and interferon-gamma on immunoglobulin E-mediated mast cell degranulation: a role for nitric oxide but not peroxynitrite or cyclic guanosine monophosphate.
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We report that cultured rat peritoneal cells spontaneously synthesize nitric oxide and this is associated with active suppression of mast cell secretory function. Addition of interleukin-4 (IL-4) or the nitric oxide synthase inhibitor N-monomethyl-l-arginine to peritoneal cells inhibited nitric oxide synthesis and enhanced anti-IgE-mediated mast cell degranulation, measured as serotonin release. Interferon-gamma (IFN-gamma) completely overcame the enhancement of serotonin release and suppression of nitrite production induced by IL-4. Over several experiments, with or without IL-4 and/or IFN-gamma, serotonin release correlated inversely with nitrite production. On a cell-for-cell basis, non-mast cells produced approximately 30 times more nitrite than mast cells in peritoneal cell populations, with or without IFN-gamma stimulation. The nitric oxide donor S-nitrosoglutathione inhibited anti-IgE-induced serotonin release from purified mast cells, whereas 8-bromo-cyclic GMP, the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, superoxide dismutase and the peroxynitrite scavenger uric acid, were without effect. We conclude that IL-4 and IFN-gamma reciprocally regulate mast cell secretory responsiveness via control of nitric oxide synthesis by accessory cells; the nitric oxide effect on mast cells is direct but does not involve cyclic GMP or peroxynitrite. (+info)
Surface and gene expression of immunoglobulin E receptors on mast cells and mast-cell numbers in interleukin-4-gene knockout mice.
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We quantified immunoglobulin E (IgE) on peritoneal mast cells of interleukin-4 (IL-4)-gene knockout (-/-) mice and wild-type (+/+) controls using a cytofluorometric method, and examined the expression of IgE receptors, estimated by quantifying the total binding of IgE on the mast cells of IL-4 (-/-) mice. The mast cells of IL-4 (+/+) mice, identified and measured using microscope fluorometry, had a fluorescence intensity five to six times higher than that of non-mast cells, while the mast cells obtained from IL-4 (-/-) mice had fluorescence intensities within the range of those of non-mast cells. Two weeks after an infection with Nippostrongylus brasiliensis, the fluorescence intensity of the mast cells of IL-4 (+/+) mice increased to a level about twice as high as that before immunization. However, no significant increase after infection was observed in IL-4 (-/-) mice. Furthermore, the mast cells of IL-4 (-/-) mice did not bind IgE when incubated with IgE at concentrations that saturated IgE receptors on the mast cells of wild-type controls, thereby indicating that the expression of IgE receptors on mast cells was impaired in the IL-4-deficient mice. Using a reverse transcription-polymerase chain reaction, we found gene expression of all three subunits (alpha-, beta- and gamma-chains) of the IgE receptor in IL-4 (-/-) like that in IL-4 (+/+) mice. The results thus suggest that the binding of IgE may be essential to induce the translation of mRNA to IgE-receptor proteins. We also observed that there were about twice as many peritoneal mast cells in the IL-4 (-/-) mice as there were in the IL-4 (+/+) mice, in both immunized and non-immunized animals. This was unexpected in view of previous findings suggesting that IL-4, in concert with stem cell factor and IL-3, stimulates the proliferation and differentiation of mast cells in vitro. (+info)