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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↗
PubMed2002

Effects of methotrexate upon inflammatory parameters induced by carrageenan in the mouse model of pleurisy.

BACKGROUND: The model of pleurisy induced by carrageenan exhibits a biphasic response (4 and 48 h) and permits the quantification of exudate, cell migration and certain enzymes such as myeloperoxidase (MPO) and adenosine-deaminase (ADA) that are markers of activated leukocytes. AIMS: The present study evaluates whether there exists, in the pleurisy model, a significant inhibition of ADA and MPO enzymes, leukocyte kinetics and other markers of inflammation [nitric oxide (NO) levels, exudation] caused by methotrexate treatment by the intraperitoneal (i.p.) route. METHODS: The pleurisy was induced by carrageenan (1%) in mice, and the parameters were analyzed 4 and 48 h after. RESULTS: After the induction of inflammation (4 h), methotrexate (20 mg/kg, i.p., 24 h before pleurisy induction) inhibited the leukocyte infiltration (p < 0.05), NO levels and MPO activity (p < 0.01), but not ADA activity and fluid leakage (p > 0.05). Regarding the second phase of pleurisy (48 h), methotrexate (40 mg/kg, i.p., 0.5 h before pleurisy induction) inhibited the leukocyte infiltration (p < 0.05), fluid leakage, NO levels (p < 0.01), and ADA and MPO activity (p < 0.05). CONCLUSIONS: These findings support the evidence that the acute administration of methotrexate has an important systemic anti-inflammatory activity in the studied inflammatory model. This effect was due to a significant inhibition on both neutrophil and mononuclear cells, being less marked in relation to exudation 48 h after. In relation to the enzymes studied and to NO levels, the findings support the evidence that methotrexate inhibits both enzymes (MPO and ADA) from leukocytes at the site of injury, thus reflecting the activation of both neutrophils and lymphocytes, respectively. Furthermore, the inhibiting effect on NO in both phases of pleurisy induced by carrageenan (4 and 48 h) indicates that methotrexate acts on constitutive and/or inducible NO synthases by means of different cells of the pleural cavity.

Adenosine Deaminase↗
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↗
PubMed2004

A case of rheumatoid arthritis exhibiting accelerating rheumatoid pleurisy during low-dose weekly methotrexate therapy.

A 75-year-old Japanese man suffering from rheumatoid arthritis (RA) had received methotrexate (MTX) treatment for 9 years and developed bilateral pleural thickening with exudative pleural effusions despite remission of the polyarthritis. A diagnosis of rheumatoid pleurisy, made by exclusion, was supported by the elevated rheumatoid factor level of the pleural fluid. The pleurisy developed concomitantly with MTX-induced leukocytopenia, and discontinuation of the MTX treatment partially improved the CRP level. These findings indicate a causal relation between the rheumatoid pleurisy and MTX and suggest that MTX therapy may be ineffective in the treatment of rheumatoid pleurisy. Treatment with 10 mg of prednisolone and 100 mg of cyclosporine A daily resulted in rapid resolution of the pleurisy. Although MTX-induced rheumatoid pleurisy is a rare condition, MTX therapy should be considered carefully in RA patients with concomitant rheumatoid pleurisy.

Journal Article↗
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↗
PubMedDate not supplied

[A comparison of the result of aspiration, needle-biopsy, pleuroscopy and thoracotomy in the diagnosis of chronic pleurisy (author's transl)].

A series of 60 diagnostic pleuroscopies was carried out in cases of isolated chronic pleurisy, or pleurisy accompanied with pleural and parenchymatous lesions. The following diagnoses were obtained : 23 non-specific chronic inflammations, 1 purulent pleurisy, 1 rheumatoid pleurisy, 25 neoplasms and 10 tuberculosis. In all cases, pleural aspiration, with bacteriology and cytotology of the fluid, as well as pleural needle-biopsy with the Abrams needle, were carried out before, with negative results in 53 cases and doubtful results in 7 cases. Later, 14 thoracotomies were carried out, either for diagnosis or for treatment (pleuro-pulmonary decortication). The diagnosis obtained by pleuroscopy was confirmed in 10 cases (5 chronic inflammations, 1 purulent pleurisy, 1 mesothelioma, 3 tuberculosis), but not confirmed in 4 cases : simple chronic inflammations related in reality to 3 neoplasms and a diagnosis of tuberculosis also due to a neoplasm. Overall, pleuroscopy allowed the diagnosis of 55 chronic pleurisies out of 60 (92%), confirmed by the progress of the disease, or later thoracotomy (10 cases). The reliability of this procedure is certain when the histology of the neoplasm or the specific condition is obtained (37 cases), but the diagnosis of chronic non-specific inflammation remains a provisional diagnosis. Exploratory thoracotomy retained its indication in this case and allowed the diagnosis to be corrected in 4 cases out of 14.

Biopsy, Needle↗
PubMed2002

[A clinical study of tuberculous pleurisy].

A clinical study of 38 patients (28 men and 10 women) with tuberculous pleurisy was conducted. The age of these patients ranged from 19 to 92 years, with an average age of 48.9 years. In 30 patients, the chief complaint was fever, and other common complaints included chest pain, dyspnea, and coughing. Bacillus tuberculosis was found in the pleural fluid of 7.9% of the patients. Tuberculous pleurisy was diagnosed histologically, based on pleural biopsy, in 23.7% of the patients. The diagnosis rate of pleural biopsy was 47.4%. There were no significant differences in results of blood and pleural fluid tests between idiopathic pleurisy and concomitant pleurisy, but the tuberculin skin test was positive in only 50% of the patients with concomitant pleurisy. The tendency was that the longer the time period between symptom onset and first examination, the greater the pleural fluid retention. The diagnosis rate of pleural biopsy was influenced by the severity of pleural fluid retention. A thoracic cavity drain was inserted for continuous drainage in 15 patients, and every patient underwent INH + RFP-based chemotherapy. Tuberculous pleurisy is an important disease among patients with pleural fluid retention, thus clinicians need to know how to treat this disease.

Adult↗
PubMed1990

[The present aspect of tuberculous pleurisy--report of the 29th series (A) of CSUCT--Cooperative Study Unit of Chemotherapy of Tuberculosis (CSUCT) of the National Sanatoria in Japan].

UNLABELLED: CSUCT carried out 9-21 month's follow up of 273 patients with exudative tuberculous pleurisy who were admitted to 39 national sanatoria in 1985, and were treated for the first time. The background factors of the patients at the time of admission were as follows: the average age, 47.2; male/female ratio 3:1; idiopathic pleurisy 163 cases and secondary pleurisy 110 cases. Distribution of maximal temperature on admission; 37.0 degrees C or less 24.4%; 37.1-38.0 degrees C 37.8%; 38.1-39.0 degrees C 28.5%; higher than 39.0 degrees C 9.3%. Younger patients tended to show higher temperature than the older. The positivity of tuberculin reaction was 84.3%, and among them 34% were strongly positive (greater than or equal to 20 mm). There was no correlation between the volume of pleural effusion and the intensity of tuberculin reaction. In patients more than 60 years of ages, the positivity was low (76.0%). The erythrocyte sedimentation rate (after 1 hour) was 63.6 +/- 31.6 mm. CLINICAL SYMPTOMS: cough in 72%; sputum in 48.5%; chest pain in 57.5%; tubercle bacilli in sputum in 11.6%. We compared idiopathic pleurisy (I) and secondary pleurisy (S) and total cases of pleurisy (T) regarding several factors; average age (I: 46.7, S: 48.0, T: 47.2); peak season of incidence (I: Feb. Mar. S: Mar. April, T: Feb. Mar. April); the period of hospitalisation (I: 4.07 months, S: 5.80 months, T: 4.77 months); the positive rate of tubercle bacilli in the pleural effusion (I: 9.0%, S: 12.9%, T: 10.5%); %VC (mean value) on admission (I: 71.4%, S: 69.8%, T: 70.7 +/- 17.0%); %VC after treatment (I: 79.0%, S: 79.7%, T: 79.4 +/- 17.9%), and we found no significant difference in the above factors between I. and S. In 49 patients who were treated by chemotherapy with steroids, %VC before treatment was 68.9% (mean value), and that after treatment was 81.2% (mean value), however, there was no significant difference between the %VC of these patients and that of total patients. Recent chemotherapy (SM or EB + INH + RFP) greatly contributed to improve clinical symptoms by accelerating the absorption of pleural effusion and in minimizing the formation of pleural thickening. Previously, we experienced often deterioration of tuberculous lesions in relation to the use of steroids. By the use of recent intensified chemotherapy, the harmful side effects of steroids became almost insignificant, and at the same time, treatment with steroids is needed only in a few cases.

Adrenal Cortex Hormones↗
PubMed1996

[Differential diagnosis of tuberculous pleurisy by the measurement of cytokine concentration in pleural effusion].

Pleural fluids obtained from 26 patients with tuberculous pleurisy (T-group), 11 with parapneumonic pleurisy (B-group) and 21 with malignant pleurisy (M-group) were tested for their biologic parameters and cytokine concentrations. 1) The average age of T-group was over 10 years lower than that of M-group with a statistically significant difference. 2) The average CRP value of B-group and the positivity on PPD skin test of T-group were higher than those of the other groups, respectively. 3) Yellowish pleural fluids were mainly observed in T- and B-group, while bloody pleural fluids were mostly seen in M-group with a statistically significant difference. The average total protein amount and adenosine deaminase value in pleural fluid significantly increased in T-group. The percentage of polymorphonuclear leukocytes showed a significant increase in B-group, while lymphocytes significantly increased in T-group with a statistically significant difference. 4) Although no significant difference in concentrations of IL-1 beta, IL-2, IFN-gamma and TNF-alpha in serum was noticed among the three groups, the average concentrations of IFN-gamma and TNF-alpha in pleural fluid in T-group were significantly higher than those in the other groups. 5) TNF-alpha-mRNA of mononuclear cells in pleural fluid was strongly expressed in 3 out of 11 patients of T-group, while no expression was observed in 6 patients of M-group. In conclusion, the measurement of concentrations of two kinds of cytokines in pleural fluid, IFN-gamma and TNF-alpha, may be clinically useful for the differential diagnosis of tuberculous pleurisy from parapneumonic pleurisy and malignant pleurisy.

Adult↗
PubMed1994

Anti-inflammatory effects of LPS, MDP and FMLP on carrageenan pleurisy in the rat.

Bacterial products fmet-leu-phe (FMLP), muramyl dipeptide (MDP) and lipopolysaccharide (LPS) were assayed for their ability to alter the inflammatory response to lambda carrageenan-induced pleurisy in Hooded Surgery rats. Continuously infused FMLP, or one initial i.v. dose of FMLP, MDP or LPS either ablated or partially suppressed the pleurisy. Total circulating leucocytes and neutrophils were suppressed by 55-65% when compared to the normal circulating leucocyte response to carrageenan pleurisy, excepting the protocol incorporating a single i.v. dose of FMLP where suppression was intermediate at 30%. There were also significant changes in the expression of FMLP receptors on circulating neutrophils. MDP and LPS induced a receptor number increase of 2 and 1.7 times initial value respectively, whilst a continuous FMLP infusion caused a receptor decrease to 0.3 times the initial value. The introduction of bacterial products at an alternative site to that of the pleurisy had an anti-inflammatory effect and the pleurisy was reduced.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed2005

Pleural fluid and serum procalcitonin as diagnostic tools in tuberculous pleurisy.

BACKGROUND: Diagnosis of tuberculous pleuritis is difficult because of its nonspecific clinical presentation and decreased efficiency of traditional diagnostic methods. We investigated the use of procalcitonin (PCT) concentration in tuberculous pleuritis diagnosis. METHODS: A prospective clinical study was performed with two different patient groups. A total of 28 patients were included: 18 with tuberculosis and 10 with nontuberculous pleurisy. Serum and pleural fluid PCT concentrations were evaluated before treatment. RESULTS: Serum and pleural fluid PCT concentrations were statistically different between tuberculous and nontuberculous pleurisy groups (P = 0.012 and P = 0.004, respectively), even though they were not elevated in relation to the cut-off level of 0.5 ng/mL. A positive and significant correlation was detected between serum and pleural fluid PCT levels (r = 0.49, P = 0.008). Diagnostic specificity and sensitivity values for serum and pleural fluid PCT in discriminating tuberculous from nontuberculous pleurisy were 80% and 72.2%, and 90% and 66.7% at the 0.081 and 0.113 ng/mL cut-off values, respectively. CONCLUSION: Relative to the current cut-off level of 0.5 ng/mL, PCT concentration is not a useful parameter for the diagnosis of tuberculous pleurisy. Because there were PCT levels in patients with tuberculous pleurisy that were below the current cut-off level but were significantly different from those of the nontuberculous group, the use of PCT should be further investigated.

Adolescent↗
PubMed2004

Additional evidence of acute anti-inflammatory effects of cyclosporin A in a murine model of pleurisy.

INTRODUCTION: It is well known that cyclosporin A (CsA) exhibits important anti-inflammatory effects, besides its immunosuppressive activity. However, the mechanisms by which CsA exerts these effects remain unclear. OBJECTIVE: This study evaluated whether the acute administration of CsA significantly interfered in leukocyte migration, exudation, myeloperoxidase (MPO) and adenosine-deaminase activities and nitrate/nitrite levels, in a mouse model of pleurisy. MATERIALS AND METHODS: Pleurisy was induced by carrageenan (1%) treatment and the parameters were analyzed 4 and 48 h after. Groups of animals were previously treated with different doses of CsA and compared with non-treated groups. RESULTS: CsA (0.1-5 mg/kg, intraperitoneal, 1 h before pleurisy induction) inhibited neutrophil migration (P<0.05), but not the exudation that occurred 4 h after pleurisy induction. At this time, CsA (1 mg/kg, 1 h before) also decreased nitrate/nitrite levels and MPO activity (P<0.01). CsA (2 mg/kg, 0.5 h before) was also effective in decreasing mononuclear influx, exudation and nitrate/nitrite levels 48 h after onset of inflammation. CONCLUSIONS: These results indicate that the acute administration of CsA is able to reduce the two leukocyte populations that occur both at 4 and 48 h after pleurisy induction, late exudation (48 h), MPO activity (4 h) and nitrate/nitrite levels (4 and 48 h). Taken together, these findings indicate that CsA has acute anti-inflammatory effects in immunocompetent animals.

Animals↗
PubMed2006

Antiinflammatory effects of Tacrolimus in a mouse model of pleurisy.

INTRODUCTION: Tacrolimus is an antibiotic macrolide with immunosuppressant properties isolated from Streptomyces tsukubaensis. OBJECTIVES: This study evaluated whether the acute and systemic administration of Tacrolimus significantly interfered in leukocyte migration, exudation, myeloperoxidase and adenosine-deaminase and nitric oxide levels, as well as Interleukin-1 (IL-1beta) and tumor necrosis factor alpha (TNFalpha) levels in a mouse model of pleurisy in comparison to those obtained with dexamethasone. MATERIALS AND METHODS: Pleurisy was induced by carrageenan (Cg, 1%), bradykinin (BK, 10 nmol), histamine (HIS, 1 micromol) or substance P (PS, 20 nmol) administered by intrapleural route (ipl.) and the inflammatory parameters (cell migration and exudation) were analyzed 4 h after. In the model of pleurisy induced by carrageenan, other markers in the pleural fluid, such as cytokines (TNFalpha and Il-1beta), nitrite/nitrate (NOx), myeloperoxidase (MPO) and adenosine-deaminase (ADA) levels, were also studied. Dexamethaseone (0.5 mg/kg, i.p., 0.5 h before) was also analyzed in all protocols. RESULTS: In the pleurisy induced by carrageenan, Tacrolimus (1 mg/kg, i.p.) and dexamethasone (0.5 mg/kg, i.p.) administered 0.5 h before caused a significant decrease in leukocytes, neutrophils and exudation (P < 0.01). Under the same conditions, Tacrolimus and dexamethasone did not modify the blood's white or red cells (P > 0.05). Tacrolimus showed a long lasting antiinflammatory effect, inhibiting leukocytes and neutrophils for up to 24 h (P < 0.01), whereas the inhibition of exudation was less marked (up to 2 h) (P < 0.01). These drugs caused a marked reduction in MPO activity, as well as IL-1beta and TNFalpha levels (P < 0.01), but only Tacrolimus inhibited ADA activity (P < 0.01). On the other hand, dexamethasone, but not Tacrolimus, inhibited NOx levels (P < 0.01). In the same conditions, Tacrolimus significantly inhibited cell migration induced by either bradykinin, histamine or substance P (P < 0.05). In a similar manner, dexamethasone inhibited leukocyte influx induced by bradykinin and histamine (P < 0.05). Regarding exudation effects, dexamethasone markedly inhibited this parameter induced by BK, HIS or SP, whereas Tacrolimus only inhibited exudation caused by HIS (P < 0.05). CONCLUSIONS: The results of the present work indicate that Tacrolimus showed important antiinflammatory properties against pleurisy in mice that are different from those caused by dexamethasone. The inhibition of proinflammatory cytokine (TNFalpha, IL-1beta), enzyme (myeloperoxidase, adenosine-deaminase) and mediator (bradykinin, histamine, substance P) release and/or action appears to account for Tacrolimus's actions.

Adenosine Deaminase↗