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)

A total of 16 episodes of peritonitis in 14 patients (9 males, 5 females), were treated with Clavulanate potentiated ticarcillin (TC), a -lactamase stable parenteral penicillin. All the pts were hospitalized and received initial loading dose of 3.2 gr intraperitoneally (i.p.) in a 6-hour 1 L exchange, which was followed by four 1 L exchanges with 320 mg/LTC. The therapy was continued for ten days. The bacteria isolated were: Staph. epid. (4), Staph. aureus (2), Strept. viridans (1), Enterococcus (1), Klebsiella Pneum. (1), Serratia (1), Enterobacter (1), Pseudomonas species: stutszeri (2), cepacia (1), fluorescens (1), negative cultures (1). Recurrence of peritonitis was seen in three patients with Pseudomonas (stutszeri (2), fluorescens (1)) peritonitis, 10-16 days after cessation of therapy. No clinical or biological side effects were seen in any patient during and/or after the therapy. These results suggest that, i.p. monotherapy of TC is effective in the treatment of CAPD peritonitis, while in cases of Pseudomonas peritonitis more specific regimens should be used.
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PMID:Treatment of CAPD peritonitis with clavulanate potentiated ticarcillin. 136 96

Mast cells are secretory cells strategically located in the vicinity of blood vessels where they can readily initiate and modulate various inflammatory processes, including plasma exudation and leukocyte infiltration. We have previously shown that 50% of the neutrophil influx during immune complex peritonitis in mice is due to mast cells. Eicosanoids are important mediators of various inflammatory processes including neutrophil infiltration. The possibility that mast cells are essential for the production of leukotrienes (LT) involved in the elicitation of neutrophils in immune complex peritonitis was investigated in mast cell-deficient, WBB6F1-W/WV, and normal, WBB6F(1-)+/+, mice. The time course and amounts of immunoreactive PGE2, 6-keto-PGF1 alpha, and TX3B2 released into the peritoneal exudates were similar in both sets of mice. LTB4 and LTC4 levels, however, were twofold higher in +/+ than in W/WV mice 2 h after stimulation. HPLC analysis of the peritoneal exudate confirmed the presence of leukotrienes. The 5-lipoxygenase inhibitor A-63162 blocked leukotriene production in a dose-dependent manner in both sets of mice. However, this compound caused a significant reduction (60%) of neutrophil infiltration only in WBB6F(1-)+/+ but not in the mast cell-deficient mice. Mast cell reconstitution of WBB6F1-W/WV mice restored the effect of A-63162 on PMN recruitment. These data suggest that mast cells in the vicinity of blood vessels are important for the synthesis of leukotrienes responsible for PMN recruitment.
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PMID:Mast cells are critical for the production of leukotrienes responsible for neutrophil recruitment in immune complex-induced peritonitis in mice. 188 Apr 19

During continuous ambulatory peritoneal dialysis (CAPD), peritoneal host defence mechanisms are repeatedly exposed to dialysis solutions (with unphysiological composition) which may compromise peritoneal immune cell functions. In this context, the current study focused on the capacity of peripheral and peritoneal PMN to release leukotrienes following exposure to conventional CAPD dialysates. PMN were obtained from peripheral blood of healthy volunteers and from the peritoneal effluent of CAPD patients with acute peritonitis. Following isolation, cells were incubated in fresh CAPD dialysates or control buffer, and calcium ionophore A23187-stimulated leukotriene synthesis was measured. Additional experiments included RP-HPLC analysis and radioactivity monitoring of lipoxygenase products in PMN labelled with 14C-arachidonic acid. Leukotriene B4 and leukotrienes C4/D4/E4 were determined by radioimmunoassay. Ionophore-triggered leukotriene release from cells exposed to control buffer was pronounced in inflammatory peritoneal PMN (70.4 +/- 31.3 ng/5 x 10(6) cells LTB4 and 13.4 +/- 19.8 ng/5 x 10(6) cells LTC4/D4/E4, mean +/- SD, n = 14) when compared to healthy peripheral PMN (26.6 +/- 16.9 ng/ml LTB4 and 6.3 +/- 6.6 ng/ml LTC4/D4/E4, n = 12). Incubation in fresh solutions for peritoneal dialysis severely depressed leukotriene release from both cell populations. These results indicate a severe inhibition of cellular responsiveness as a consequence of dialysate exposure which could contribute to the impairment of host defence early in the CAPD cycle.
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PMID:Leukotriene release from peripheral and peritoneal leukocytes following exposure to peritoneal dialysis solutions. 192 11

A continuous ambulatory peritoneal dialysis patient developed eosinophilic peritonitis and was followed for 7 months. After 1 month, the peritonitis resolved, with a concomitant drop in percentage of hypodense eosinophils (Eos) recovered from peritoneal dialysate (PD) as well as a drop in fluid major basic protein levels. Blood eosinophil differential percentages were low, but the percentage of hypodense Eos in the blood tended to be relatively increased. Stool samples showed no evidence of parasitic infection, and epicutaneous skin tests were negative. Leukotriene C4 levels remained relatively constant as did white blood cell counts. Flow cytometric analysis of lymphocytes and granulocytes from PD and blood revealed high levels of CD23-positive lymphocytes.
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PMID:Characterization of eosinophils in a continuous ambulatory peritoneal dialysis patient with eosinophilic peritonitis. 193 18

Peritoneal macrophages isolated from CAPD patients phagocytosed S. epidermidis in a time dependent manner. Coincident with a maximum phagocytic uptake of 56% by 12 hours, there was secretion of a significant amount of neutral protease (1.37 +/- 0.2 mg [3H]-casein degraded/10(6) cells, P = 0.05). In contrast to these delayed effects, coincubation of PMO with S. epidermidis resulted in a significant increase in both LTB4 and LTC4 synthesis above that of controls, with 6.33 +/- 1.20 ng LTB4/10(6) cells (P less than 0.01) and 2.06 +/- 0.68 ng LTC4/10(6) cells (P = 0.014) being generated by three hours. The generation of these lipoxygenase products was both time and dose dependent, and the rapid production and release of the potently chemotactic LTB4 is consistent with the observed clinical response, where a rapid influx of PMN into the peritoneal cavity occurs during episodes of peritonitis, while the generation of LTC4 may contribute to the hyperemia and interstitial edema. In contrast, although there was a time dependent rise in cyclooxygenase product generation by unstimulated cells, a dose dependent inhibition of synthesis was clearly demonstrated when cells were incubated with bacteria, with a mean 40% reduction in generation of PGE2 and a mean 34% reduction in TXB2 generation (P = 0.01 and P less than 0.025, respectively). It was demonstrated that the inhibition was not due to lack of available substrate and that the generation of eicosanoids was unrelated to phagocytosis, bacterial/PMO contact or bacterial surface characteristics. Instead, the observed effect of S. epidermidis on the PMO was attributable to a secreted bacterial product.
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PMID:Eicosanoid synthesis in human peritoneal macrophages stimulated with S. epidermidis. 211 61

From 1975 to 1987, we had 56 patients of septic shock in the Department of Surgery. Multiple organ failure occurred in many septic patients. Glucocorticoids inhibited the secretion of chemical mediators (histamine, serotonin and bradykinin) and then prevented septic shock. Intravenous administration of dexamethasone showed no change in amounts of leukotrienes (LTC4, LTD4, LTE4) in venous blood in peritonitis rats. Dexamethasone treatment of septic rats corrected FDP and nearly normalized PEP values. When glucocorticoid was given intravenously at the time of cecal incision, PFKase, PKase, G6Pase and PEPCK were stimulated, respectively. Protease inhibitor FUT-175 was infused in 5% dextrose (0.1mg/ml/hr) in septic rats. Survival time was 12.1 +/- 2.3 hour in FUT-175 group and 6.6 +/- 1.1 hr without FUT-175. In FUT-175 injected rats G6P decreased by 20%, FDP increased 50% and lactate doubled. PEP levels increased 30% above peritonitis values. The amounts of leukotrienes (LTC4, LTD4, LTE4) in venous blood were gradually decreased by pretreatment with the specific 5-lipoxygenase inhibitor AA-861 after peritonitis. Specific treatments in septic shock should be instituted administration of glucocorticoid, antibiotics, protease inhibitor and lipoxygenase inhibitor. The importance of septic shock as a factor contributing to organ failure must be acknowledge. We believe that the prompt and efficacious treatment of septic shock is the best therapy.
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PMID:[Effects of anti-toxic agents in septic shock]. 258 23

Production and release of arachidonic acid (AA) compounds (eicosanoids: prostaglandins-cyclooxygenase and leukotrienes-lipoxygenase) and monokines (TNF-alpha, IL-1 and others) play an essential role in the expression of antitumour activity of macrophages (MO). We investigated the possibility of inducing the antitumour activity of peritoneal murine and human MO by regulating their production of eicosanoids and monokines. The antitumour activity of MO was inversely correlated to production of PGE2 and directly correlated to production of leukotrienes (LTC4 and LTD4). Thus, indomethacin rendered murine MO cytostatic against tumour cells and enhanced the antitumour activity of human peritoneal macrophages from renal patients on CAPD (continuous ambulatory peritoneal dialysis), and leukotriene inhibitors (NDGA-nordihydroguaiaretic acid and AA861) prevented antitumour cytostatic activity of MO. Human peritoneal MO collected during periods of inflammation (infectious peritonitis) were more active against tumour cells, especially when cultured in the presence of LPS, and their activity was correlated to increase with the release of TNF and of IL-1 beta. Human peritoneal MO from inflammation-free patients reacted against a human tumour cell line if cultured with LPS and TPA (phorbol-myristate acetate) and were therapeutically effective against the same palpable s.c. tumours implanted in nude mice.
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PMID:Modulation of antitumour activity of macrophages by regulation of eicosanoids and cytokine production. 792 85

The anatomic aspect of peritonitis describes the division of the abdominal cavity into the supracolic, infracolic and paracolic spaces, moreover the lesser sac and the cul-de-sac of the pelvis. Physiologically the peritoneum plays an important role in the passive exchange of fluid and absorption of particles. Endotoxin, which is elaborated by bacteria activates the classical as well as the alternative complement pathway. It activates also the arachidonic acid metabolism, leading to the release of prostaglandins (PG) and leukotriens (LTC). The local host defense against a bacterial invasion includes the activation of cellular and humeral immunologic defense mechanism, in which the final product of the complement pathway (C5b-9), as well as chemoattractants C3a, C5a and C567 play a key role.
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PMID:Anatomic, physiologic, bacteriologic and immunologic aspects of peritonitis. 938 97

Stimulated mast cells release a variety of chemotactic factors such as tumor necrosis factor alpha (TNF-alpha) and leukotriene B4. Recent studies have shown that mast cell-derived TNF-alpha plays a critical role in host defense against Gram negative bacterial infections by the recruitment of neutrophils to the sites of infection. In the present study, we sought to investigate if mast cells release leukotriene (LT) B4 in response to bacteria and, if so, to establish its in vivo relevance. We show that mast cells release significant amounts of LTB4 and LTC4 in response to exposure to FimH-expressing type 1 fimbriated Escherichia coli in vitro. To test the functional significance of mast cell-derived LTs during an E. coli infection in vivo, we examined the effect of a LT-synthesis inhibitor, A-63162, on bacterial clearance and neutrophil influx in an infectious peritonitis model in mast cell-deficient mice (WBB6F1-W/WV) and their normal congenic control (WBB6F1-+/+) mice. Our results show that a treatment with A-63162 reduced neutrophil influx and bacterial clearance in the peritoneal cavities of mast cell-sufficient but not -deficient mice. Thus, mast cell-derived LTs contribute to host defense by mediating early neutrophil influx and bacterial clearance at sites of infection.
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PMID:Role of mast cell leukotrienes in neutrophil recruitment and bacterial clearance in infectious peritonitis. 1085 57

Leukotrienes are derived from arachidonic acid and serve as mediators of inflammation and immediate hypersensitivity. Leukotriene B(4) (LTB(4)) and leukotriene C(4) (LTC(4)) act through G protein-coupled receptors LTB(4) receptor (BLTR) and Cys-LTR, respectively. To investigate the physiological role of BLTR, we produced mice with a targeted disruption of the BLTR gene. Mice deficient for BLTR (BLTR(-/-)) developed normally and had no apparent hematopoietic abnormalities. Peritoneal neutrophils from BLTR(-/-) mice displayed normal responses to the inflammatory mediators C5a and platelet-activating factor (PAF) but did not respond to LTB(4) for calcium mobilization or chemotaxis. Additionally, LTB(4) elicited peritoneal neutrophil influx in control but not in BLTR(-/-) mice. Thus, BLTR is the sole receptor for LTB(4)-induced inflammation in mice. Neutrophil influx in a peritonitis model and acute ear inflammation in response to arachidonic acid was significantly reduced in BLTR(-/-) mice. In mice, intravenous administration of PAF induces immediate lethal anaphylaxis. Surprisingly, female BLTR(-/-) mice displayed selective survival (6 of 9; P = 0.002) relative to male (1 of 11) mice of PAF-induced anaphylaxis. These results demonstrate the role of BLTR in leukotriene-mediated acute inflammation and an unexpected sex-related involvement in PAF-induced anaphylaxis.
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PMID:Targeted disruption of the leukotriene B(4) receptor in mice reveals its role in inflammation and platelet-activating factor-induced anaphylaxis. 1093 35


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