Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postsplenectomy bacterial sepsis may be fatal, due to defects in both cellular and humoral immune responses. The objective of this study was to assess the efficacy of peritoneal macrophage antibacterial function in the early postsplenectomy period. Murine models of splenectomy and sham operation were characterized and peritoneal macrophages were harvested 24 h to 1 wk after surgery. Cells from splenectomized animals demonstrated a nonsignificant delay in phagocytosis of Escherichia coli at 24 h with, however, significantly impaired killing of intracellular organisms at 24 h and 1 wk compared to the sham group. Paradoxically, the production of the macrophage antibacterial product superoxide anion was not impaired at either time point in the splenectomy group compared with sham-operated and control mice. Nitric oxide release was significantly lower in the splenectomized group (p = 0.006), a possible explanation for reduced bacterial killing. Mortality from bacterial peritonitis was significantly higher with concomitant splenectomy than in the sham splenectomy group at 24 h (p < 0.02). The production of TNF from macrophages was up-regulated immediately following splenectomy, a cytokine which may contribute to mortality from bacteremic shock. Local defects in macrophage antimicrobial function may contribute significantly to bacteremia and to subsequent mortality in the early postsplenectomy period.
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PMID:Characterization of the defects in murine peritoneal macrophage function in the early postsplenectomy period. 760 13

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

Nitric oxide plays an important role in mediating the inflammatory process. The aim of this study was to evaluate if nitric oxide production was increased during peritonitis in patients receiving continuous ambulatory peritoneal dialysis (CAPD), and the association with the prognosis. The study population comprised 21 patients with 22 episodes of peritonitis. Fifteen patients without peritonitis were controls. Nitrate was measured by HPLC and nitrite by the Griess method, to reflect nitric oxide production. Peritoneal dialysate effluent and plasma were collected from six patients during peritonitis and 1 week after treatment to study changes in dialysate:plasma ratio. In 15 patients, nitrite was measured during peritonitis and every 3 days for 2 weeks or until normalized for evolutional changes. The dialysate:plasma ratios of nitrate and nitrite during peritonitis were reduced 26% and 41.5%, respectively, after 1 week of treatment, indicating the peritoneal production of nitric oxide during peritonitis. In the evolutional study, a 5.1-fold increase of peak nitrite levels in bacterial peritonitis (n = 13) and a 2.5-fold increase in fungal peritonitis (n = 3) were observed compared to controls. Nitrite gradually declined to control levels (9.3 +/- 7.2 days) after effective antibiotic treatment, but took longer than to normalize leukocyte count in the peritoneal dialysate effluent (3.9 +/- 1.9 days). In four patients with refractory peritonitis (Candida infection in three, Acinetobacter infection in one), the nitrite levels remained elevated 2-fold despite treatment, and the catheters were removed. It is concluded that nitrite levels in peritoneal dialysate effluent may serve as a marker to assess treatment efficacy in CAPD patients with peritonitis.
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PMID:Peritoneal nitric oxide is a marker of peritonitis in patients on continuous ambulatory peritoneal dialysis. 901 24

To gain insights into the amino acid metabolism and L-arginine-nitric oxide system, we studied 21 control continuous peritoneal dialysis (CPD) patients and 13 patients with 15 episodes of acute peritonitis. The concentrations of amino acids, including L-arginine, were measured in the peritoneal dialysate and in the serum. The data demonstrate that patients with end-stage renal disease on CPD who have acute peritonitis develop L-arginine deficiency. The majority of patients with acute bacterial peritonitis have increased nitric oxide production as judged by the level of nitrites in the dialysate. The recovery from peritonitis is associated with a decline in nitric oxide generation. Paradoxically, there is a smaller subgroup of these patients that shows low nitrite levels during acute peritonitis. The nitrite to L-arginine ratio in the peritoneal dialysate is increased in patients with peritonitis, further suggesting the development of substrate deficiency. These findings implicate L-arginine as a conditionally essential amino acid in CPD patients with acute peritonitis and raise questions concerning the necessity of L-arginine supplementation.
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PMID:Amino acid profile and nitric oxide pathway in patients on continuous ambulatory peritoneal dialysis: L-arginine depletion in acute peritonitis. 915 5

Nitric oxide production was studied in cirrhotic patients with spontaneous bacterial peritonitis (SBP) or with other infections. We followed up on the time course of serum nitrate levels in 51 hospitalized patients aged between 34 and 81 years. Four groups were defined: patients with SBP (group 1, n = 14), patients with bacteremia (group 2, n = 11), patients with urinary tract infection (group 3, n = 11) and patients in a stable clinical condition (group 4, n = 20). The four groups did not differ in terms of Pugh score (11 +/- 1, 10 +/- 1, 11 +/- 1, and 10 +/- 1, respectively). Serum nitrate levels averaged 31 +/- 2 micromol/L in group 4 (84 samples). On the day results of cytobacteriological examination were positive, mean serum nitrate levels were 75 +/- 17, 63 +/- 9, and 36 +/- 9 micromol/L, respectively, in groups 1 (17 cases), 2 (11 cases), and 3 (11 cases) (P < .001). The maximum nitrate values recorded during follow-up were higher in groups 1 (149 +/- 15 micromol/L) and 2 (112 +/- 11 micromol/L) than in group 3 (66 +/- 7 micromol/L; P < .001 and < .01, respectively). These maximum values were recorded in all groups approximately 2 weeks after the infection was diagnosed. The mean duration of NO overproduction, as defined by nitrate level (3)90 micromol/L, was 15 +/- 3 days in group 1 and 5 +/- 1 day in group 2. When the nitrate concentration was studied in serum and ascitic fluid sampled on the same day, it was found to be higher in ascitic fluid than in serum in eight cases of SBP in the period preceding the peak serum nitrate concentration (100 +/- 17 vs. 63 +/- 14 micromol/L; P < .001). Our data indicate that SBP in cirrhotic patients led to a long-lasting increased local production of NO. This overproduction may contribute to maintaining splanchnic vasodilation and thus worsen the hyperkinetic state in these patients.
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PMID:Long-lasting NO overproduction in cirrhotic patients with spontaneous bacterial peritonitis. 918 47

Deficient production of nitric oxide may be responsible for the defective defense barrier and persistence of bacterial infection. To gain insight into amino acid-metabolism and L-arginine-nitric oxide system, we studied 34 end-stage renal disease (ESRD) patients on peritoneal dialysis (PD) (20 males, 14 females, with a mean age of 53.5 years and a mean duration on PD of 29.7 months). The concentrations of amino acids, including L-arginine, were measured in peritoneal dialysate and in the serum. The data demonstrated that patients with ESRD on PD have normal serum amino-acid profiles, whereas those with acute peritonitis develop L-arginine deficiency (from 99 +/- 9 to 52 +/- 9 mumol/L). In addition, levels of asparagine, glycine, proline (nonessential) as well as valine, threonine, and lysine (essential) were reduced in patients with peritonitis. The majority of patients with acute bacterial peritonitis have increased nitric oxide production as judged by the level of nitrites in the dialysate (36 +/- 2 vs 57 +/- 6 mumol/L). The recovery from peritonitis was associated with a decline in nitric-oxide generation. There was a smaller subgroup of these patients that showed paradoxically low nitrite levels during acute peritonitis. The nitrite: L-arginine ratio in the peritoneal dialysate was increased in patients with peritonitis, further suggesting the development of substrate deficiency. These findings implicate L-arginine as a conditionally essential amino acid in PD patients with acute peritonitis. Further studies are needed to address the issue of L-arginine supplementation in such patients.
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PMID:Decreased L-arginine during peritonitis in ESRD patients on peritoneal dialysis. 936 Jun 82

Nitric oxide (NO) is a messenger molecule involved in pathogen suppression. Cirrhosis is characterized by an increased risk for infections, including spontaneous bacterial peritonitis (SBP). The role of NO in the infections that develop in cirrhosis has not been clearly established. The aim of this study was to investigate the utility of measuring ascites NO in the diagnosis of SBP and/or in determining the predisposition of cirrhotic patients to develop this infection. Nitric oxide metabolites (nitrites + nitrates [NOx]) were measured by chemiluminescence in 105 ascites samples obtained from 87 cirrhotic patients and in 87 simultaneously obtained serum samples. Ascites NO levels were not significantly different among ascites from patients with SBP (n = 39; median, 48 micromol/L), patients with sterile ascites (n = 54; median, 42 micromol/L), and samples obtained after patients with SBP had been treated (n = 12; median, 62 micromol/L). No differences in ascites NO levels were observed between culture-positive and culture-negative peritonitis. Among 50 patients with sterile ascites on initial paracentesis, 7 patients developed peritonitis during follow-up; no differences in baseline NO levels were observed between patients who developed peritonitis (median, 46 micromol/L) and those who did not (median, 41 micromol/L). Among patients with SBP, mortality was significantly higher in those with NO levels >60 micromol/L. A very significant direct correlation was found between ascites and serum NO levels (r2 = .86). In conclusion, ascites NO levels in cirrhotic patients are not useful either to diagnose or to determine predisposition to SBP. Rather, ascites NO levels reflect serum levels, are higher in cirrhotic patients with more severe liver disease, and may be a useful prognostic marker.
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PMID:The diagnostic and predictive value of ascites nitric oxide levels in patients with spontaneous bacterial peritonitis. 965 91

Nitric oxide (NO) is produced by various cell types, and it is an important mediator in many biological processes, including macrophage-mediated cellular host defense. The relevance and amount of NO production in peritonitis during peritoneal dialysis (PD) treatment is still not clear. We studied whether human peritoneal macrophages (PMphi) isolated from healthy PD patients or PD patients with peritonitis showed different spontaneous or lipopolysaccharide (LPS)/interferon gamma (IFN-gamma)-induced NO production (LPS, 1 ng/mL-10 microg/mL; IFN-gamma, 10-1000 U/mL; incubation between 6-48 hours; measured by Griess reagent). Results were compared with human blood monocytes (HBM) isolated from buffy coats. Inducible nitric oxide synthetase (iNOS) mRNA expression was looked for in PMphi by reverse transcriptase polymerase chain reaction (RT-PCR). Furthermore, plasma (P) and peritoneal dialysate effluent (D) nitrite concentrations were measured in vivo. The dialysate-to-plasma ratio (D/P) of nitrite concentration was inverse in the case of peritonitis compared to infection-free patients (peritonitis D/P = 1.3, non peritonitis D/P = 0.4; p < 0.01). PMphi from peritonitis patients produced higher amounts of NO than did those from infection-free patients (0.040+/-0.044 nmol per microgram cell protein versus 0.018+/-0.015 nmol per microgram cell protein, p < 0.05). NO release could not be further enhanced by stimulation with LPS plus IFN-gamma (1 ng/mL, 250 U/mL, respectively). However, NO production in PMphi from infection-free patients increased during in vitro stimulation (0.044+/-0.031 nmol per microgram cell protein versus 0.018+/-0.015 nmol per microgram cell protein, p < 0.01). An increase of iNOS mRNA expression could be demonstrated by RT-PCR. Blood monocytes from healthy donors also increased NO release during cytokine stimulation (0.032+/-0.015 nmol per microgram cell protein versus 0.019+/-0.009 nmol per microgram cell protein, p < 0.05). Our results indicate that significant amounts of NO are released intraperitoneally in the case of bacterial peritonitis. PMphi represent a site of NO production, though the absolute amounts released in vitro are only moderate. NO production can be induced in PMphi and HBM by LPS/IFN-gamma stimulation in vitro.
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PMID:Nitric oxide production in peritoneal macrophages from peritoneal dialysis patients with bacterial peritonitis. 1040 50

The present study assessed whether peritoneal macrophages isolated from cirrhotic patients produce nitric oxide (NO) and express NO synthase type II (NOS II) mRNA and protein. Patients with cirrhosis and ascites without peritonitis or with unresolved or resolved spontaneous bacterial peritonitis (SBP) were studied. Following paracentesis, ascites NO(2)(-) + NO(3)(-) content (NOx) was measured. Peritoneal macrophages from ascites were seeded on well plates, and NO(2)(-) in the medium was determined. NOx was higher in patients with unresolved or resolved SBP than in cirrhotic patients without peritonitis. Macrophages of patients with SBP or resolved SBP produced NO(2)(-) after 30 hours in culture, but those obtained from patients without peritonitis did not. Reverse-transcription polymerase chain reaction (RT-PCR) and immunocytochemical analysis revealed the presence of a clear signal for NOS II mRNA and protein in macrophages of SBP patients, regardless of whether or not the infection subsided. Therefore, peritoneal macrophages isolated from cirrhotic patients with unresolved or resolved SBP produce NO and express the NOS II mRNA and protein, suggesting that NOS II may contribute to the control of SBP, or to its associated pathology, in human cirrhosis.
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PMID:Nitric oxide production and inducible nitric oxide synthase expression in peritoneal macrophages of cirrhotic patients. 1046 73

We previously described a long-lasting overproduction of nitric oxide (NO) in cirrhotic patients with spontaneous bacterial peritonitis. The aim of the present study was to investigate the presence of the inducible NO pathway in peritoneal macrophages. Ascitic fluids were collected from 29 patients with cirrhosis, aged between 35 and 82 years. Peritoneal macrophages were isolated and cultured in the presence or absence of 1 microg/ml lipopolysaccharide and/or 500 units/ml interferon-gamma (IFN-gamma) for 6 days. NO production was measured as nitrate+nitrite (NO(x)), inducible NO synthase (iNOS) protein expression was analysed by immunocytochemistry and Western blot analysis using a specific anti-(human iNOS) antibody, and the catalytic activity of NOS was revealed by cytochemical staining for NADPH-dependent diaphorase. Cultured macrophages spontaneously released small amounts of NO(x) [median (10-90th percentile) of 18 separate experiments: 3.3 (0-8) micromol/l]. Addition of lipopolysaccharide alone or in combination with IFN-gamma to the culture medium did not change the levels of NO(x), while IFN-gamma alone dramatically increased NO production [13.4 (3.5-28.3) micromol/l; P<0.001]. Macrophages were stimulated by IFN-gamma to a greater extent in patients with recent spontaneous bacterial peritonitis (n=13) than in those in a stable clinical condition (n=18) [19.8 (10.5-30.1) and 10.0 (3.2-14.5) micromol/l respectively; P<0.001]. Macrophages freshly isolated or stimulated with IFN-gamma expressed iNOS protein, as shown by Western blot and immunocytochemical analysis, and stained for NADPH diaphorase. Our findings demonstrate the presence of iNOS protein in peritoneal macrophages from cirrhotic patients. The role of IFN-gamma appears to be a determinant for the up-regulation of NO production, particularly under conditions of infection. Therefore peritoneal macrophages producing large amounts of NO at the site of infection may contribute to maintaining splanchnic vasodilation in these patients.
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PMID:Up-regulation of nitric oxide production by interferon-gamma in cultured peritoneal macrophages from patients with cirrhosis. 1049 39


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