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

We studied the protective effect of anti-tumor necrosis factor-alpha (anti-TNF) polyclonal antibody on phosphoenolpyruvate carboxykinase (PEPCK) expression in lipopolysaccharide-induced endotoxemia and peritonitis sepsis induced by cecal incision. At 3 h after intraperitoneal lipopolysaccharide injection, levels of serum glucose, liver glycogen, and PEPCK expression were decreased and serum TNF was elevated. In contrast, 3 h after cecal incision, levels of serum glucose, serum TNF, and PEPCK expression were elevated. At 6 h after cecal incision (terminal sepsis), serum TNF remained elevated and levels of serum glucose, liver glycogen, and PEPCK expression were decreased. Circulating TNF was not detected in septic and endotoxemic rats pretreated with anti-TNF. Passive immunization with rat anti-TNF antibody restored PEPCK expression in early endotoxemia and sepsis (3 h), but not in terminal sepsis (6 h). Anti-TNF failed to reverse sepsis-induced hypoglycemia and hyperglycemia, suggesting that besides TNF, some other mediators are involved in glucose dyshomeostasis.
 ...
PMID:Efficacy of anti-tumor necrosis factor polyclonal antibody on phosphoenolpyruvate carboxykinase expression in septic and endotoxemic rats. 882 86

Interleukin-4 (IL-4) demonstrates properties in vitro that suggest an anti-inflammatory role in the immune response, one of which is the inhibition of tumor necrosis factor-alpha (TNF) release. We examined the effects of IL-4 administration on mortality and serum TNF levels in two murine models of peritonitis. Animals infected with intraperitoneal injections of Escherichia coli and Bacteroides fragilis (acute peritonitis) had a decreased mortality and earlier TNF-alpha peak when pretreated with 5,000 units IL-4. Animals infected with bacteria and a sterile fecal adjuvant (chronic peritonitis) had no alteration in mortality or serum TNF levels (which were consistently low) with IL-4 pretreatment. These data demonstrate that, under some in vivo conditions, IL-4 can significantly ameliorate a septic insult, but this effect appears to be highly model-dependent and not clearly related to its effects on TNF-alpha.
 ...
PMID:Interleukin-4 prevents mortality from acute but not chronic murine peritonitis and induces an accelerated tumor necrosis factor-alpha response. 883 69

The efficacy of intraperitoneal instillation of antimicrobial agents in eliminating the bacterial contaminant in patients with generalized peritonitis remains controversial. We determined the effect of intraperitoneal instillation of taurolidine or imipenem on mortality, and on the concentration of bacteria, endotoxin, and tumor necrosis factor (TNF) in rats with intraperitoneally injected bacteria. Thirty rats were inoculated intraperitoneally with two enteric bacterial strains, followed by either taurolidine, saline, or imipenem. Abdominal fluid and blood were analyzed at different time intervals. The survival rate was highest in the imipenem group (p < 0.05). The bacterial concentration in abdominal fluid in the taurolidine and imipenem group was lower than in the saline group (p < 0.005), but the concentration in the imipenem group was lowest (p < 0.005). The endotoxin concentration in abdominal fluid and plasma in the taurolidine group was lower than in the other two groups (p < 0.05). The TNF concentration in abdominal fluid and plasma in the taurolidine group was lower than in the saline group (p < 0.05), whereas the concentration in the imipenem group was higher (p < 0.005). We conclude that topically applied taurolidine in rats with intraperitoneally injected bacteria may have a weak antibacterial effect, and lowered concentrations of endotoxin and TNF. Topically applied imipenem had a profound bactericidal activity but induced endotoxin and TNF release.
 ...
PMID:Effect of intraperitoneal antimicrobials on the concentration of bacteria, endotoxin, and tumor necrosis factor in abdominal fluid and plasma in rats. 888 Jan 24

Although the role of members of the Enterobacteriaceae and anaerobes in the pathogenesis of intra-abdominal infections has been extensively demonstrated, the role played by enterococci in these infections remains controversial. The pathophysiological mechanisms induced by enterococci in intra-abdominal infection were studied in a nonfatal model of peritonitis in rats by implanting a gelatin capsule containing Escherichia coli and Bacteroides fragilis with or without increasing concentrations of Enterococcus faecalis or heat-inactivated enterococci. The ability of the rat peritoneal cavity to sterilize itself after bacterial challenge was evaluated by quantifying the inflammatory response in the peritoneal cavity, reflected by both phagocyte and cytokine responses. Effects were evaluated 6, 12, and 24 h and 3 and 6 days after inoculation. On day 6 after inoculation, the highest enterococcal concentration (10(8) CFU/ml) was accompanied by significantly increased concentrations of E. coli in peritoneal fluid and peritoneal phagocytes when compared to other groups. In the first 12 h after inoculation, tumor necrosis factor and interleukin-6 concentrations were significantly increased in the peritoneal fluid of the animals that had received the highest inoculum of enterococci or heat-inactivated enterococci. In the late period of the study (3 and 6 days), significantly increased leukocyte counts were observed in the peritoneal fluid of these animals. These results suggest that E. faecalis somehow inhibited phagocytosis and intracellular killing of the other pathogens and also played an inflammatory role, which might account for the bacterial synergy observed in this model.
 ...
PMID:Evidence of the proinflammatory role of Enterococcus faecalis in polymicrobial peritonitis in rats. 897 4

We have previously described cross-reactive antilipopolysaccharide (anti-LPS), or anti-endotoxin, monoclonal antibodies (MAbs) which provide cross-protection in several systems of endotoxin bioactivity. The protective effects of the murine cross-reactive MAb WN1 222-5 (immunoglobulin G2a(kappa) [IgG/2a(kappa)]) and of its chimerized version, SDZ 219-800 [human IgG1(kappa)], have now been evaluated in lethality models against LPS from three different serotypes and in bacterial infection models. We confirmed the protective activity of the two MAbs in D-galactosamine-sensitized mice challenged with LPS of other E. coli serotypes (O18, O127, and O111). The protective effect correlated with the suppression of tumor necrosis factor formation. Furthermore, WN1 222-5 enhanced bacterial clearance of intravenously administered E. coli O111 bacteria, thus protecting mice from death. However, the MAbs were unable to provide protection in a peritonitis model (intraperitoneal inoculation). Our study, therefore, shows that LPS cross-reactive antibodies are capable of mediating cross-protection against LPS and bacteria but that the selected models have a clear influence on the results.
 ...
PMID:Similarities and disparities between core-specific and O-side-chain-specific antilipopolysaccharide monoclonal antibodies in models of endotoxemia and bacteremia in mice. 900 48

The selectins are inducible adhesion molecules critically important for the inflammatory response. We investigate here the functional effects of three monoclonal antibodies (MoAbs) raised against murine E-selectin (9A9, 10E6, and 10E9.6) on neutrophil recruitment in vivo, leukocyte rolling and circulating leukocyte concentrations in vivo, and adhesion of myeloid cells to E-selectin transfectants and recombinant E-selectin-IgG fusion protein in vitro. MoAbs 9A9 and 10E6 map to the lectin and epidermal growth factor (EGF)-like domains of murine E-selectin, whereas 10E9.6 binds to the consensus repeat region. 10E9.6 blocked neutrophil recruitment in a model of thioglycollate-induced peritonitis in Balb/c mice by more than 90% but had no effect in C57BL/6 mice. 9A9 and 10E6 blocked neutrophil recruitment in this assay only when combined with a P-selectin antibody, 5H1. Neither 9A9 nor 10E9.6 alone blocked leukocyte rolling in tumor necrosis factor-alpha-treated venules of Balb/c mice, but 9A9 almost completely inhibited leukocyte rolling when combined with the function-blocking murine P-selectin MoAb, RB40.34. In contrast, 10E9.6 had no effect on leukocyte rolling in RB40.34-treated Balb/c or C57BL/6 mice. 10E9.6 did not affect adhesion of myeloid cells to E-selectin transfectants or attachment, rolling, and detachment of myeloid cells to murine E-selectin-IgG fusion protein. However, adhesion was completely blocked in the same assays by 9A9. Taken together, these results indicate that E-selectin serves a function, other than rolling, that appears to be critically important for neutrophil recruitment to inflammatory sites in Balb/c mice.
 ...
PMID:Differential effect of E-selectin antibodies on neutrophil rolling and recruitment to inflammatory sites. 910 22

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.
 ...
PMID:PECAM-1 expression in human mesothelial cells: an in vitro study. 915 26

In this study, we investigated whether the recently identified lectin-like domain of tumor necrosis factor (TNF) is implicated in its biological activities on mammalian cells. To this end, a mouse TNF (mTNF) triple mutant, T104A-E106A-E109A mTNF (referred to hereafter as triple mTNF), lacking the lectin-like affinity of mTNF for specific oligosaccharides, was compared with the wild-type molecule for various TNF effects in vitro and in vivo. The triple mTNF displayed a 50-fold-reduced TNF receptor 2 (TNFR2)-mediated bioactivity but only a 5-fold-reduced TNFR1-mediated bioactivity in vitro. The specific activity of the triple mutant on L929 fibrosarcoma cells was slightly reduced compared with that of the wild type. We subsequently assessed the systemic toxicity of triple versus wild-type mTNF, since TNFR2 is partially implicated in this activity. The triple mTNF had a significantly reduced toxicity compared with that of wild-type mTNF in vivo. Moreover, we compared the effects of the triple and the wild-type mTNFs in TNFR1-mediated phenomena, such as (i) induction of tolerance towards a lethal mTNF dose and (ii) protective activity in cecal ligation and puncture-induced septic peritonitis. No significant differences between the mutant and wild-type forms were observed. In conclusion, these results indicate that triple mTNF, lacking TNF's lectin-like binding capacity, has reduced systemic toxicity but retains the tolerance-inducing and peritonitis-protective activities of wild-type mTNF.
 ...
PMID:Generation of a mouse tumor necrosis factor mutant with antiperitonitis and desensitization activities comparable to those of the wild type but with reduced systemic toxicity. 916 25

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.
 ...
PMID:Peritoneal dialysis effluent, cytokine levels, and peritoneal mesothelial cell viability in CAPD: a possible relationship. 936 Jun 42

During systemic infection, the serum lipopolysaccharide binding protein (LBP) binds to the lipid A component of bacterial endotoxins and facilitates its delivery to the CD 14 receptor on the cell surface of macrophages, where proinflammatory cytokines are released. There is no knowledge to date whether LBP is also present in the effluent of patients with continuous ambulatory peritoneal dialysis (CAPD)-associated peritonitis. We investigated the dialysis effluent of 37 patients with CAPD peritonitis for immunoreactive LBP, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-1 beta and compared the findings with the cytokine levels in 20 noninfected CAPD patients. The mean +/- SEM concentrations of LBP, TNF-alpha, and IL-1 beta were significantly higher in the effluent of patients with peritonitis than in noninfected CAPD effluent. In comparison to controls (0.23 +/- 0.05 microgram/mL), LBP was 0.68 +/- 0.13 microgram/mL in the effluent of patients with CAPD-associated infectious peritonitis. For TNF-alpha, levels were 0.50 +/- 0.25 pg/mL in the control effluent versus 124.7 +/- 46.6 pg/mL in the effluent of peritonitis patients. For IL-1 beta the levels were 0.24 +/- 0.14 pg/mL in the control effluent and 71.23 +/- 17.53 pg/mL in the peritonitis patients. Our findings demonstrate that LBP is significantly elevated in the effluent of CAPD patients during an episode of CAPD-associated peritonitis and might be used as a marker of intraperitoneal bacterial infection.
 ...
PMID:Lipopolysaccharide binding protein: a marker for intraperitoneal bacterial infection in patients with CAPD peritonitis. 936 Jun 83


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>