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At least 19 recordsLinked to original sources
PubMed1987

Differential effects of anti-inflammatory drugs on fluid accumulation and cellular infiltration in reverse passive arthus pleurisy and carrageenan pleurisy in rats.

At 4 h following induction of pleural inflammation in rats using either an immune stimulus (reverse passive Arthus reaction, RPAR) or a chemical stimulus (carrageenan), the cellular infiltration and fluid accumulation responses were quantitated. The bell-shaped antigen (BSA) dose-response curve describing the fluid response was increased upward as the anti-BSA dose was increased from 0.25 to 1 mg, whereas the dose-response curve for cellular infiltration was both shifted upward and to the right. Both nonsteroidal anti-inflammatory drugs and a mixed lipoxygenase-cyclooxygenase inhibitor (BW 755C) preferentially inhibited fluid accumulation in RPAR pleurisy elicited with 5 mg BSA and 1 mg anti-BSA and in carrageenan pleurisy. In contrast, these drugs inhibited cellular infiltration preferentially in RPAR pleurisy elicited with 1 mg BSA and 1 mg anti-BSA. These results demonstrate that the fluid and cellular responses in rat pleural inflammation can be differentially regulated by anti-inflammatory drugs depending upon the doses of antigen and antibody employed in RPAR pleurisy and the identity of the inflammatory stimulus.

Animals↗
PubMed1989

[T-lymphocyte subsets in peripheral blood and pleural effusion in tuberculous pleurisy and carcinomatous pleurisy: analysis by monoclonal antibodies].

By using monoclonal antibodies, OKT8(pant), OKT4(inducer/helper),OKT8(suppressor/cytotoxic) T-lymphocyte subsets were examined in 25 patients with tuberculous pleurisy and 15 patients with carcinomatous pleurisy. The results showed that percent and absolute counts of OKT8,OKT4,OKT8 in tuberculous pleural effusion were significantly higher than those in carcinomatous pleural effusion. Percent and absolute counts of OKT8, OKT4, in tuberculous pleural effusion were significantly higher than those in peripheral blood. OKT8% in peripheral blood of carcinomatous pleural effusion was significantly lower than that in peripheral blood of control group. When OKT8% greater than 65, OKT4% greater than 45, OKT8 number/mm8 greater than 1,000, OKT4 number/mm8 greater than 800, OKT8 number/mm8 greater than 500 in pleural effusion, it suggests pleural effusion is tuberculous. when OKT8% less than 55, OKT4% less than 45, OKT5 number/mm8 less than 500, OKT4 number/mm8 less than 300, OKT8 number/mm8 less than 200, it suggests pleural effusion is carcinomatous pleural effusion.

Adenocarcinoma↗
PubMed1982

Effects of anti-inflammatory drugs on triple vaccine-induced pleurisy in rats.

Effects of various anti-inflammatory drugs on triple vaccine-induced pleurisy, a model of delayed hypersensitivity, were examined and compared with those on carrageenin-induced pleurisy in rats. Steroidal drugs depressed markedly the volume of exudate and the number of leucocytes in both types of pleurisy. Gold compounds also depressed both types of pleurisy. Non-steroidal anti-inflammatory drugs were apt to show depressive effects on carrageenin-induced pleurisy, especially on increased exudate volume. BW755C produced a depressive effect on carrageenin-induced pleurisy, but on triple vaccine-induced pleurisy, BW755C produced only a slight depressive effect. Cyproheptadine produced a slight depressive effect on carrageenin-induced pleurisy, but not on triple vaccine-induced pleurisy. Promethazine had a slight depressive effect on both types of pleurisy. D-penicillamine and levamisole did not show any depressive effects on triple vaccine-induced pleurisy. The results show that reported mediators in carrageenin-induced pleurisy (prostaglandin, serotonin, leukotriene B, etc.) are not relevant to triple vaccine-induced pleurisy. Specific lymphokines and/or degradated products of complement may participate in the latter. This triple vaccine-induced pleurisy seems to be a good model for screening non-steroidal anti-inflammatory drugs which have steroidal-like activity.

Animals↗
PubMed1997

Differential diagnosis of tuberculous pleurisy by measurement of cytokine concentrations in pleural effusion.

STUDY OBJECTIVE: Measurement of cytokine concentration in serum and pleural effusion may be useful in the differential diagnosis of tuberculous pleurisy. PATIENTS AND METHODS: We compared the biochemical properties and concentrations of cytokines in serum and pleural effusion samples of 18 patients with tuberculous pleurisy, 7 patients with parapneumonic pleurisy, and 25 patients with malignant pleurisy. RESULTS: A high value of adenosine deaminase (ADA) was observed in pleural effusion of patients with tuberculosis. The serum concentrations of interleukin (IL)-1-beta, IL-2, interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha were similar among the three groups. However, the concentration of IFN-gamma in pleural effusion was high in tuberculous patients, and that of TNF-alpha was high in tuberculous and parapneumonic pleural fluid, but both cytokines were low in malignant pleural fluid. The sensitivity, specificity and accuracy of IFN-gamma in the diagnosis of tuberculous pleurisy were 94%, 100% and 98%, respectively. Similarly, those of TNF-alpha for the diagnosis of infectious pleurisy including tuberculous and parapneumonic pleurisy were 88%, 80% and 84%, respectively. CONCLUSIONS: Our results indicate that simultaneous measurement of IFN-gamma and TNF-alpha in pleural effusion is a useful diagnostic tool for differentiating tuberculous pleurisy from parapneumonic and malignant pleurisy.

Adult↗
PubMed1986

Roles of leukotrienes in two rat allergic inflammatory models; IgE-mediated and IgG-antigen complex-induced pleurisies.

Rat IgE pleurisy was induced by the injection of di-nitrophenol-conjugated bovine serum albumin (DNP-BSA) 48 hours after the intrapleural injection of rat anti-DNP-IgE serum. IgG-BSA complex pleurisy was also induced by the intrapleural injection of IgG-BSA complexes produced at the optimum ratio in vitro. Plasma exudation was markedly increased in the first 20 minutes, but not observed thereafter, in IgE pleurisy, whereas marked plasma exudation in the first 20 minutes was followed by weak exudation at three and five hours in IgG-BSA complex pleurisy. Leukotrienes (LTs) E4 (100 ng/rat), D4 (32) and B4 (16) were detected on HPLC in the pleural exudate in the first 20 minutes of IgG-BSA complex pleurisy, but less (9 ng/rat) LTE4 alone was detected in the five-hour exudate. The first 20-minute pleural exudate contained 13 ng/rat of LTE4 in IgE pleurisy. The plasma was completely inhibited by simultaneous treatment of rats with pyrilamine (2.5 mg/kg, i.p.) and methysergide (3 mg/kg, i.p.), as it was in compound 48/80-induced pleurisy. In IgG-BSA complex pleurisy, 90% of the pleural exudate for the first 20 minutes was inhibited by the same treatment, and the rest was completely suppressed by simultaneous treatment with an intrapleural injection of AA-1777, a selective 5-lipoxygenase inhibitor. AA-1777 alone did not reduce the plasma exudation significantly. The 5-lipoxygenase inhibitor was also very effective in reducing the migrating numbers of polymorphonuclear and mononuclear leukocytes to half, without affecting the eosinophils of mast cells.

Animals↗
PubMed1998

Characterization of the receptor and the mechanisms underlying the inflammatory response induced by des-Arg9-BK in mouse pleurisy.

1 The characterization of the B1 kinin receptor, and some mediators involved in the inflammatory response elicited by intrathoracic (i.t.) administration of des-Arg9-bradykinin (BK) in the mouse model of pleurisy, was investigated. 2 An i.t. injection of des-Arg9-BK (10-100 nmol per site), a selective B1 agonist, caused a significant and dose-related increase in the vascular permeability observed after 5 min, which peaked at 1 h, associated with an increase in cell influx, mainly neutrophils, and, to a lesser extent, mononuclear cell influx, peaking at 4 h and lasting for up to 48 h. The increase in fluid leakage caused by des-Arg9-BK was completely resolved 4 h after peptide injection. I.t. injection of Lys-des-Arg9-BK (30 nmol per site) caused a similar inflammatory response. 3 Both the exudation and the neutrophil influx elicited by i.t. injection of des-Arg9-BK were significantly antagonized (P<0.01) by an i.t. injection of the selective B1 antagonists des-Arg9-[Leu8]-BK (60 and 100 nmol per site) or des-Arg9-NPC 17731 (5 nmol per site), administered in association with des-Arg9-BK (P<0.01), or 30 and 60 min before the cellular peak, respectively. In contrast, an i.t. injection of the B2 bradykinin selective receptor antagonist Hoe 140 (30 nmol per site), at a dose which consistently antagonized bradykinin (10 nmol per site)-induced pleurisy, had no significant effect on des-Arg9-BK-induced pleurisy. 4 An i.t. injection of the selective tachykinin receptor antagonists (NK1) FK 888 (1 nmol per site), (NK2) SR 48968 (20 nmol per site) or (NK3) SR 142801 (10 nmol per site), administered 5 min before pleurisy induction, significantly antagonized neutrophil migration caused by i.t. injection of des-Arg9-BK. In addition, FK 888 and SR 142801, but not SR 48968, also prevented the influx of mononuclear cells in response to i.t. injection of des-Arg9-BK (P<0.01). However, the NK3 receptor antagonist SR 142801 (10 nmol per site) also significantly inhibited des-Arg9-BK-induced plasma extravasation. An i.t. injection of the calcitonin gene-related peptide (CGRP) receptor antagonist CGRP8-37 (1 nmol per site), administered 5 min before pleurisy induction, inhibited des-Arg9-BK-induced plasma extravasation (P<0.01), without significantly affecting the total and differential cell migration. 5 The nitric oxide synthase inhibitors L-NOARG and L-NAME (1 pmol per site), administered 30 min beforehand, almost completely prevented des-Arg9-BK (i.t.)-induced neutrophil cell migration (P<0.01), and, to a lesser extent, mononuclear cell migration (P<0.01). The D-enantiomer D-NAME had no effect on des-Arg9-BK-induced pleurisy. At the same dose range, L-NOARG and L-NAME inhibited the total cell migration (P<0.01). L-NAME, but not L-NOARG caused significant inhibition of des-Arg9-BK-induced fluid leakage. Indomethacin (1 mg kg(-1), i.p.), administered 1 h before des-Arg9-BK (30 nmol per site), inhibited the mononuclear cell migration (P<0.05), but, surprisingly, increased the neutrophil migration at 4 h without interfering with plasma extravasation. The administration of terfenadine (50 mg kg(-1), i.p.), 30 min before des-Arg9-BK (30 nmol per site), did not interfere significantly with the total cell migration or with the plasma extravasation in the mouse pleurisy caused by i.t. injection of des-Arg9-BK. 6 Pretreatment of animals with the lipopolysaccharide of E. coli (LPS; 10 microg per animal, i.v.) for 24 h did not result in any significant change of the inflammatory response induced by i.t. injection of des-Arg9-BK compared with the saline treated group. However, the identical treatment of mice with LPS resulted in a marked enhancement of des-Arg9-BK induced paw oedema (P<0.01). 7 In conclusion, we have demonstrated that the inflammatory response induced by i.t. injection of desArg9-BK, in a murine model of pleurisy, is mediated by stimulation of constitutive B1 receptors. (These responses are largely mediated by release of neuropeptides such as substanceP or CGRP and also by NO, but products derived from cyclo-oxygenase pathway and histamine seem not to be involved. Therefore, these results further support the notion that the B1 kinin receptor has an important role in modulating inflammatory responses, and it is suggested that selective B1 antagonists may provide therapeutic benefit in the treatment of inflammatory and allergic conditions.

Animals↗
PubMed1986

Difference in the in vitro metabolism of leukotrienes in the exudates from allergic and nonallergic rat pleurisies.

The metabolism of leukotrienes (LTs) in the cell-containing inflammatory exudate of rat pleurisy was studied in vitro. The exudates of both nonallergic carrageenin-induced pleurisy and IgG immune complex-mediated pleurisy converted 3H-LTB4 to 20-OH LTB4, but virtually did not metabolized 3H-LTC4 or 3H-LTE4 up to 2 hrs. 3H-LTD4 was changed to LTC4 by the exudate of non-allergic pleurisy, whereas 3H-LTD4 was metabolized to LTE4 by that of allergic pleurisy. Reflecting on the different metabolism, the gamma-glutamyl transpeptidase activity in the exudate of carrageenin-induced pleurisy was significantly higher than that in IgG immune complex mediated pleurisy. The enzyme activity was not derived from the blood itself, but from the infiltrated polymorphonuclear leukocytes. The activity of the cell homogenate in both exudates was not significantly different. Thus, it could be concluded that the difference in the metabolism of LTD4 between the nonallergic and allergic pleural exudates in vitro was mainly attributable to the enhanced activity of the gamma-glutamyl transpeptidase released in the exudate.

Animals↗
PubMed1996

Anti-inflammatory effects of theophylline, cromolyn and salbutamol in a murine model of pleurisy.

1. The aim of this study was to examine the effect of theophylline, cromolyn and salbutamol, three well-known anti-asthmatic drugs, on the early (4 h) and late (48 h) phases of cell migration and fluid leakage induced by carrageenin in the pleural cavity of mice. 2. In the first set of experiments, animals were pretreated (30 min) with different doses of theophylline (0.5-50 mg kg-1, i.p.), cromolyn (0.02-0.2 mg per pleural cavity) or salbutamol (0.05-50 mg kg-1, i.p.); the total and differential cell content, and also the exudate were analysed 4 h after carrageenin (1%) administration. Afterwards, in order to evaluate the time course effects of these drugs on both phases of the inflammatory reaction, one dose employed in the above protocol was chosen, to pretreat (0.5-24 h) different groups of animals. The studied parameters were evaluated 4 and 48 h after pleurisy induction. 3. Acute administration of theophylline (1-50 mg kg-1, i.p.) cromolyn (0.02-0.2 mg per pleural cavity) and salbutamol (0.5-50 mg kg-1, i.p.), 30 min prior to carrageenin, caused significant inhibition of total cell and fluid leakage in the pleural cavity at 4 h (P < 0.01). All drugs exerted a long-lasting inhibitory effect on both exudation and cell migration (P < 0.01) when administered 0.5-8 h before pleurisy induction. However, the temporal profile of the inhibitory effect induced by these drugs on the first phase of the inflammatory reaction was clearly different. Thus, the inhibitory effect induced by theophylline and cromolyn on exudation was significantly longer (up to 24 h) in comparison to their effects on cell migration (only up to 8 h). In contrast, although salbutamol when administered 30 min before pleurisy induction abolished fluid leakage (P < 0.01), this effect was not sustained in the groups pretreated for 4-8 h. In these latter groups, a significant but much smaller reduction of exudation was observed (P < 0.01), whereas the magnitude of cell migration inhibition did not vary. 4. The second phase (48 h) of the inflammatory reaction induced by carrageenin (1%) was significantly inhibited by cromolyn (0.02 mg per pleural cavity) when this drug was administered 0.5-24 h before pleurisy induction (P < 0.01). Similar results were observed when theophylline (50 mg kg-1, i.p.) was administered 0.5-4 h before the injection of the phlogistic agent (P < 0.01). Treatment of the animals with salbutamol (5 mg kg-1, i.p.), 0.5-24 h before pleurisy induction, did not inhibit either cell migration or fluid leakage. In this condition, a significant increase of these parameters was observed in the group pretreated with salbutamol 8-24 h before pleurisy induction (P < 0.01). 5. These results indicate that theophylline and cromolyn were able to inhibit the early (4 h) and late (48 h) phases of the inflammatory reaction induced by carrageenin in a murine model of pleurisy. Salbutamol was effective only against the early phase. The inhibitory effects of theophylline, cromolyn and salbutamol on the early phase of this inflammatory reaction were long-lasting, although a distinct profile of inhibition was observed among them. These findings confirm and extend previous results described in other models of asthma and support both clinical and experimental evidence suggesting that these anti-asthmatic agents exhibit marked anti-inflammatory properties.

Albuterol↗
PubMed1980

Comparison of the effect of phenylbutazone, desonide and cyclophosphamide on four types of experimental pleurisy.

The action of phenylbutazone, a non-steroid anti-inflammatory drug, desonide, a corticosteroid, and cyclophosphamide, an immunosuppressant agent, was studied on four types of experimental pleurisy: carrageenan-pleurisy in rats; passive reversed Arthus pleurisy in rats; Bordetella pertussis-delayed hypersensitivity pleurisy in rats and PPD (purified protein derivative)--delayed hypersensitivity pleurisy in guinea-pigs. For each compound, the action on the exudate and on the number of the different categories of leucocytes in the inflammation focus was evaluated. In carrageenan-inflammation, phenylbutazone reduced the oedema and the number of neutrophils and macrophages. Its favourable effect on exudative events in Arthus--and B. pertussis--reactions was not accompanied by high modifications at the cellular level. With the exception of PPD-pleurisy, desonide reduced the three other reactions. Its action related to the exudate and the various leucocyte types, except in the Arthus reaction in which only the number of neutrophils was decreased. The effect of cyclophosphamide was mainly in B. pertussis pleurisy in which it resulted in a decrease of oedema and a reduction in the number of mononuclears. For each compound, correlations between the effect on exudative and cellular phenomena are discussed.

Animals↗
PubMed1989

Pleural fluid neuron-specific enolase. A useful diagnostic marker for small cell lung cancer pleurisy.

We studied the value of pleural fluid neuron-specific enolase as a possible diagnostic marker for pleurisy of small cell lung cancer by using enzyme immunoassay. Pleural fluid NSE levels in 12 patients with carcinomatous pleurisy due to small cell lung cancer were compared with those in 37 patients with carcinomatous pleurisy due to non-small cell lung cancer and 39 patients with tuberculous pleurisy. The pleural fluid NSE level was elevated in nine of 12 (75 percent) patients with SCLC. However, only two of 37 (5 percent) patients with NSCLC and two of 39 (5 percent) patients with tuberculous pleurisy had an elevated pleural fluid NSE level. Moreover, none of ten SCLC patients with cytology-negative pleural effusions showed elevated pleural fluid NSE level. Thus, determination of pleural fluid NSE levels seems to be an effective means to differentiate carcinomatous pleurisy due to SCLC from that due to NSCLC, tuberculous pleurisy and cytology-negative pleural effusion in SCLC.

Carcinoma, Non-Small-Cell Lung↗
PubMed1997

[Analysis of chemical mediators involved in acute inflammatory reaction with the rat pleurisy model].

Mediators involved in acute inflammation were explored by using rat pleurisies induced by carrageenin or zymosan. The kallikrien-kinin system and eicosanoids were the main mediators responsible for plasma exudation in carrageenin-induced rat pleurisy, while histamine, PAF and the complement system could be the main mediators involved in the vascular permeability increase to cause plasma exudation into the pleural cavity in zymosan-induced rat pleurisy. Several chemokines were detected in the pleural exudates of carrageenin-pleurisy as well as those of zymosan-pleurisy; and exogenous recombinant TNF alpha, IL-1, IL-6 and CINC induced neutrophil migration into rat pleural cavity. These results suggest that these chemokines, directly or indirectly, may partly cause neutrophil migration in the pleural exudates during carrageenin- and zymosan-induced pleurisy. In addition, chemokine production in response to prostanoids and PAF production in response to arachidonic acid were also suggested.

Animals↗
PubMed1990

[The significance of pleural fluid cytology in the differential diagnosis of pleurisy showing lymphocyte-predominant pleural effusion].

We examined the significance of pleural fluid cytology in differentiation between tuberculous and non-tuberculous pleurisy in patients with lymphocyte-predominant pleural effusion. We divided pleural fluid cytologic findings into two patterns, that is "tuberculous" and "non-tuberculous pattern", according to the report by Spieler, and compared the cytologic pattern with the final clinical diagnosis. Thirteen out of 19 cases (68.4%) with tuberculous pleurisy showed "tuberculous pattern" in the pleural fluid cytology, while four (pleurisy associated with collagen-vascular disease, asbestosis and carcinoma, and idiopathic pleurisy) out of 13 (30.8%) with non-tuberculous pleurisy revealed "tuberculous pattern". The pleural fluid cytology could be used as one of the additional means to differentiate between tuberculous and non-tuberculous pleurisy, though it is impossible to differentiate between them with the pleural fluid cytology alone.

Diagnosis, Differential↗
PubMed1985

Rat pleurisy induced by kaolin or croton oil: time course of fluid accumulation and white cell migration.

Rat pleurisy was induced by intrapleural injection of 0.1 ml of 1% kaolin or 1% croton oil, and the time courses of pleural fluid accumulation and white cell migration were examined. Peak pleural fluid accumulation was observed at respectively 5 and 16 h after the inciter injection. Migration of white cells into the pleural cavity showed a peak at respectively 7 or 24 h after each inciter. Polymorphonuclear leukocytes were predominant in pleural cells of kaolin pleurisy at 3 h, while in croton-oil pleurisy the major white cells were mononuclear cells and lymphocytes at 3 h, and polymorphonuclear leukocytes appeared later around 16 h. Pretreatment with several agents modified both types of induced pleurisy. Kaolin pleurisy at 3 h was suppressed by indomethacin, mefenamic acid, paramethasone, bromelain and soy-bean trypsin inhibitor, while croton oil pleurisy at 3 h was suppressed significantly by indomethacin and paramethasone.

Animals↗