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

In vitro secretion of the prostanoids PGE2 and PGI2 and of the cytokine IL-1 beta by peritoneal macrophages obtained from CAPD patients during episodes of peritonitis and infection free periods, was determined, after culturing with or without 5 micrograms/ml of LPS. The release of PGE2 and PGI2 as measured by its stable metabolite 6-keto-PGF alpha was determined in 10 episodes of peritonitis and 10 infection free periods. IL-1 beta release was determined in 14 episodes of peritonitis and 20 infection free periods. PGI2 release from macrophages declined sharply during peritonitis both in the absence and presence of LPS in the culture medium (p less than 0.005). A tendency to decreased PGE2 release was found during peritonitis, when macrophages were cultured in the absence of LPS. In the presence of LPS, the same amounts of PGE2 were released during peritonitis and during an infection free period. On the other hand, peritoneal macrophages released significantly more IL-1 beta during peritonitis as compared to an infection free period, provided that the cells were in vitro stimulated with LPS. In view of the interregulatory effects between prostanoids and macrophage cytokines in their production, these findings may indicate that the impaired release of PGI2 during peritonitis has allowed the macrophages to secrete more IL-1 beta after in vitro stimulation with LPS. This implies that PGI2 and PGE2 may play a distinct role in the regulation of cytokine secretion by these cells.
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PMID:Peritoneal macrophages from patients on continuous ambulatory peritoneal dialysis show a differential secretion of prostanoids and interleukin-1 beta. 143 64

Recent evidence suggests that pentoxifylline (PTX) may be useful in the treatment of sepsis. We examined effects of PTX in a conscious swine model of sepsis. Yucatan minipigs (20-30 kg) were anesthetized and instrumented with catheters in the vena cava, aortic arch, pulmonary artery (Swan-Ganz thermodilution catheter), and peritoneum. Twenty-four hours after surgery, sepsis was induced by intraperitoneal (ip) injection of Escherichia coli bacteria (2 x 10(10) cfu/kg). Nonseptic pigs received intraperitoneal saline (5 ml/kg). PTX treatment (3 mg/kg/hr, iv; 1 mg/ml in 0.9% saline) and maintenance fluid (5 ml/kg/hr, iv) were started with bacterial infusion. An additional 60 cc/kg 0.9% saline bolus was administered iv at 1 hr. Pigs were monitored before and 1, 2, 5, and 24 hr after bacterial injection. Intraperitoneal injection of bacteria led to significant reductions in blood pressure and cardiac output and elevations in pulmonary wedge pressure and pulmonary vascular resistance. These effects were attenuated by PTX treatment. All septic animals demonstrated elevated creatinine, blood urea nitrogen, circulating endotoxin (LPS), and tumor necrosis factor concentrations, reductions in white blood cell and platelet counts, and peritonitis. None of these responses was altered by PTX treatment. We conclude that PTX may prove to be a useful therapeutic tool in the early treatment of septic shock but is limited in the scope of its effects.
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PMID:Pentoxifylline treatment of sepsis in conscious Yucatan minipigs. 144 87

The production of TNF-alpha, IL-1, and IL-6 was measured in mice after bolus i.v. Escherichia coli O111 LPS injections and during bacteremia induced either by bolus i.v. or by i.p. challenges of live E. coli O111. High but transient TNF-alpha peaks were observed after bolus i.v. LPS or bacterial challenges. In contrast, the levels during lethal peritonitis increased progressively to values 50- to 100-fold lower than the peak values observed after i.v. injections, and remained sustained until death. Whereas after i.v. challenge with 1000 LD50 of LPS, anti-TNF-alpha antibody fully protected mice from death and reduced serum IL-1 and IL-6 levels, anti-TNF-alpha antibody did not improve the survival of mice nor reduced serum IL-1 and IL-6 levels after i.p. bacterial challenge. In contrast to anti-TNF-alpha antibodies, anti-LPS antibodies were protective in the peritonitis model. Protection was accompanied by a striking reduction of bacterial numbers and of TNF-alpha, IL-1, and IL-6 levels in the serum, but the levels of these cytokines were only marginally affected in the peritoneal lavage fluid. This latter observation demonstrates that the local peritoneal cytokines did not diffuse readily into the circulation, thus suggesting that at least part of the circulating cytokines are produced systemically. In conclusion, the striking differences between cytokine profiles as well as the divergent efficacy of anti-TNF-alpha antibody after i.v. bolus and after i.p. challenges suggest that TNF-alpha may not be as important in the pathogenesis of lethal peritonitis than after lethal acute bacteremia.
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PMID:Cytokine production after intravenous or peritoneal gram-negative bacterial challenge in mice. Comparative protective efficacy of antibodies to tumor necrosis factor-alpha and to lipopolysaccharide. 154 27

We have reported previously that macrophages obtained from renal patients on continuous ambulatory peritoneal dialysis (CAPD) during an episode of infectious peritonitis display a decrease in intracellular cAMP levels and in spontaneous in vitro release of PGE2 and PGI2. Such macrophages also release large quantities of IL-1 beta and TNF alpha when stimulated in vitro by LPS. In view of the interregulatory effects between PGE2 and macrophage cytokines (IL-1 beta and TNF alpha) in their production, we examined in the present work to what extent the LPS-induced release of either IL-1 beta or TNF alpha in vitro from CAPD-originated peritoneal macrophages is affected by graded doses of exogenous PGE2 (range 0-1000 ng/ml) and by the cyclooxygenase inhibitor indomethacin (INDO) (10(-6) M). IL-1 beta and TNF alpha were determined using an enzyme-linked immunoabsorbent assay and an immunoradiometric assay, respectively. We found that PGE2 invariably induced a dose-dependent decrease in TNF alpha release. In peritoneal macrophages collected during an infection-free period, TNF alpha release decreased from 3225 pg/ml (controls) to 353 pg/ml at 1000 ng/ml of PGE2, and in peritoneal macrophages collected during an episode of infectious peritonitis, it decreased from 4100 pg/ml (controls) to 545 pg/ml at 100 ng/ml of PGE2. However, PGE2 failed to influence the secretion of IL-1 beta. INDO induced an approx. two-fold increase in TNF alpha release, but had no effect on IL-1 beta release. These findings indicate that exogenous and endogenous PGE2 controls the release of TNF alpha rather than IL-1 beta from LPS-stimulated peritoneal macrophages.
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PMID:Prostaglandin E2 inhibits the release of tumor necrosis factor-alpha, rather than interleukin 1 beta, from human macrophages. 154 34

Elevated systemic levels of tumor necrosis factor (TNF) have been directly correlated with increased mortality during experimental gram-negative bacterial sepsis. Although monoclonal antibodies (mAbs) directed against gram-negative bacterial lipopolysaccharide (endotoxin, LPS) decrease TNF production in vitro and enhance survival in vivo, the precise relationship between inhibition of TNF secretion and protective capacity has not been defined. We hypothesized that protective anti-LPS mAbs inhibited LPS-stimulated TNF production. To test this hypothesis, we first produced and characterized three anti-LPS mAbs. We then examined the ability of these mAbs to decrease TNF secretion in an in vitro assay using cells from the murine macrophage cell line RAW 264.7. Subsequently, we assessed the protective capacities of these anti-LPS mAbs in a murine mucin peritonitis model of sepsis using live Escherichia coli 0111:B4 bacterial challenge. Our results demonstrated that those anti-LPS mAbs that decreased LPS-stimulated TNF secretion in vitro were protective in vivo. We concluded that inhibition of TNF secretion in vitro reflected protective capacity and that anti-LPS mAbs may confer protection via abrogation of macrophage TNF secretion. Inhibition of TNF production in vitro may provide a valuable test that may facilitate the selection of protective anti-LPS mAbs.
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PMID:Protective anti-lipopolysaccharide monoclonal antibodies inhibit tumor necrosis factor production. 159 69

We have reported previously that human peritoneal macrophages collected from patients on Continuous Ambulatory Peritoneal Dialysis (CAPD) during an episode of peritonitis secrete increased amounts of interleukin-1 (IL-1), as compared to those collected during an infection free period, provided the cells were stimulated in vitro by LPS. We now report that such macrophages release also higher amounts of Tumor Necrosis Factor (TNF), if collected during peritonitis and stimulated subsequently in vitro by LPS. The increase in release of TNF was ascertained by radio-immunoassays as well as by bioassay of cytostatic effect against the highly sensitive TNF target-cell line L929 murine transformed fibroblasts. The present reported results, in addition to previously reported data on release of IL-1, indicate that induction of release of cytokines from human peritoneal macrophages is a dual stepwise process: first priming in vivo in an inflammatory environment and, secondly stimulation in vitro by LPS.
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PMID:Peritoneal macrophages from patients on continuous ambulatory peritoneal dialysis have an increased capability to release tumour necrosis factor during peritonitis. 166 36

The in vitro release of interleukin-1 beta (IL-1 beta) by peritoneal macrophages from CAPD patients was studied during 16 infection free periods (16 patients) and 13 episodes of peritonitis (10 patients) using an ELISA. Without exogeneous stimulation with LPS, peritoneal macrophages released the same amounts of IL-1 beta. irrespective if they were obtained during an infection free period (473 +/- 92 pg/ml 24h, means +/- SEM) or during peritonitis (324 +/- 125 pg/ml). However, in response to a dose of 5 micrograms/ml of LPS, peritoneal macrophages released significantly more (p less than 0.005) IL-1 beta during peritonitis (6155 +/- 1743 pg/ml). These findings show that during peritonitis, peritoneal macrophages are primed in vivo to release more IL-1 beta in vitro after stimulation with LPS, indicating that activation of peritoneal macrophages for IL-1 beta secretion occurs stepwise.
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PMID:Peritoneal macrophages from patients on CAPD show an increased capacity to secrete interleukin-1 beta during peritonitis. 198 87

Continued improvement in outcome in ICU patients with the hypermetabolism-organ failure syndrome require a better understanding of the disease process. Current research is focusing on altered regulation at the cell membrane and nuclear levels. Cell culture models have provided insight into one possible mechanism, that of altered cell-cell communication with dysregulation of the associated parenchyma. Alteration of the PUFA content of the membrane of macrophages with omega 3 PUFA can be easily induced and maintained, and can alter cell membrane physical characteristics and how the membrane responds to LPS-stimulated prostanoid release. There is also an associated alteration in the release of monokine. These changes are associated with improvements in T lymphocyte response to antigen and in outcome from septic peritonitis. The precise mechanisms through which these effects occur are the subject of investigations, as are the clinical implications. Nonetheless, nutrient pharmacology with omega 3 PUFA may be a promising area of research that will have clinical applicability in ICU patients.
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PMID:Omega 3 polyunsaturated fatty acids as modulators of cellular function in the critically ill. 202 Jun 14

Interleukin-1 (IL-1) release by peritoneal macrophages obtained from patients on continuous ambulatory peritoneal dialysis (CAPD) was studied in nine patients during an infection-free period and eight patients during an infectious peritonitis, using an ELISA for IL-1 beta. Without exogenous stimulation with LPS, peritoneal macrophages from infected and uninfected patients released the same amounts of IL-1 beta, 183 +/- 40 pg ml-1 24 h-1) per 10(6) cells (means +/- SEM) and 251 +/- 96 pg ml-1, respectively. However, in response to a dose of 5 micrograms ml-1 of LPS, peritoneal macrophages released significantly more (P less than 0.005) IL-1 beta during peritonitis (6579 +/- 2793 pg ml-1 24 h-1 per 10(6) cells) compared with the infection-free period (1040 +/- 182 pg ml-1). These findings show that after microbial invasion of the peritoneal cavity, peritoneal macrophages are primed in vivo to release an increased amount of IL-1 beta in vitro after subsequent exogenous stimulation with LPS, indicating that peritoneal macrophage activation for IL-1 beta secretion occurs in steps.
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PMID:Endotoxin-stimulated peritoneal macrophages obtained from continuous ambulatory peritoneal dialysis patients show an increased capacity to release interleukin-1 beta in vitro during infectious peritonitis. 212 5

In 18 intensive care patients the effect of a IgG-Anti-Lipopolysaccharide (Anti-LPS), was investigated in a randomized study following surgery after bacterial infections, mostly peritonitis. Fresh frozen plasma was administered during the first 5 postoperative days, containing either more than 65 micrograms/ml Anti-LPS in the therapy group or less than 12.5 micrograms/ml in the control group. The serum level of Anti-LPS was monitored. Clinical and chemical parameters were recorded to evaluate infectious complications and outcome of the patients. The mortality in the treatment group was not different from the control group with 30% (3 out of 10) and 25% (2 out of 8), respectively. No beneficial effect was observed either from the administration of Anti-LPS or from endogenously produced Anti-LPS on any clinical parameter in our patients.
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PMID:Anti-lipopolysaccharide-immunoglobulin (IgG-anti-LPS) therapy in intensive care patients following surgery from infectious disease. 221 Aug 65


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