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Molecules (Basel, Switzerland) May 2020Nootkatone (NTK) is a sesquiterpenoid found in essential oils of many species of (Rutaceae). Considering previous reports demonstrating that NTK inhibited inflammatory...
Nootkatone (NTK) is a sesquiterpenoid found in essential oils of many species of (Rutaceae). Considering previous reports demonstrating that NTK inhibited inflammatory signaling pathways, this study aimed to investigate the effects of this compound in mice models of acute and chronic inflammation. Murine models of paw edema induced by carrageenan, dextran, histamine, and arachidonic acid, as well as carrageenan-induced peritonitis and pleurisy, were used to evaluate the effects of NTK on acute inflammation. A murine model of granuloma induced by cotton pellets was used to access the impact of NTK treatment on chronic inflammation. In the acute inflammation models, NTK demonstrated antiedematogenic effects and inhibited leukocyte recruitment, which was associated with decreased vascular permeability, inhibition of myeloperoxidase (MPO), interleukin (IL)1-β, and tumor necrosis factor (TNF)-α production. In silico analysis suggest that NTZ anti-inflammatory effects may also occur due to inhibition of cyclooxygenase (COX)-2 activity and antagonism of the histamine receptor type 1 (H). These mechanisms might have contributed to the reduction of granuloma weight and protein concentration in the homogenates, observed in the chronic inflammation model. In conclusion, NTK exerted anti-inflammatory effects that are associated with inhibition of IL1-β and TNF-α production, possibly due to inhibition of COX-2 activity and antagonism of the H1 receptor. However, further studies are required to characterize the effects of this compound on chronic inflammation.
Topics: Acute-Phase Reaction; Animals; Anti-Inflammatory Agents; Capillary Permeability; Carrageenan; Cotton Fiber; Cyclooxygenase 2; Disease Models, Animal; Edema; Female; Granuloma; Histamine; Inflammation; Interleukin-1beta; Leukocytes; Male; Mice; Molecular Docking Simulation; Peritonitis; Peroxidase; Pleurisy; Polycyclic Sesquiterpenes; Receptors, Histamine; Tumor Necrosis Factor-alpha
PubMed: 32392744
DOI: 10.3390/molecules25092181 -
The Medical Journal of Malaysia Jun 2008
Topics: Amebiasis; Humans; Lung Diseases, Parasitic; Male; Middle Aged; Pleurisy
PubMed: 18942313
DOI: No ID Found -
Arthritis and Rheumatism Aug 1962
Topics: Arthritis; Arthritis, Rheumatoid; Humans; Medical Records; Pleurisy
PubMed: 13909174
DOI: 10.1002/art.1780050404 -
The European Respiratory Journal Oct 1997Although infectious, inflammatory and neoplastic diseases frequently involve the pleural space and walls, little is known about the immunological and molecular... (Review)
Review
Although infectious, inflammatory and neoplastic diseases frequently involve the pleural space and walls, little is known about the immunological and molecular mechanisms underlying pleural disorders. This article provides an overview of recent insights into immunobiological processes likely to play a role in the pathogenesis of pleural disorders. Pleural involvement in certain diseases is associated with the infiltration of a number of different types of immune cells, such as neutrophils, eosinophils or lymphocytes, in various proportions depending on both the course and the aetiology of the underlying disease. In addition to infiltrating cells, mesothelial cells have been demonstrated to actively participate in pleural inflammation via release of various mediators and proteins, including platelet-derived growth factor (PDGF), interleukin-8, monocyte chemotactic peptide (MCP-1), nitric oxide (NO), collagen, antioxidant enzymes and the plasminogen activation inhibitor (PAI). Furthermore, several inflammatory mediators have been detected at increased concentrations within pleural effusions, including lipid mediators, cytokines and proteins (adenosine deaminase, lysosyme, eosinophil-derived cationic proteins, and products of the coagulation cascade). The presence of these mediators underline the concept of pleural inflammation, and certain cytokines seem to characterize a specific aetiology of pleurisy. The understanding of these processes and the sequence of events leading to pleural loculation, pleural adhesion or repair are likely to provide the basis for early therapeutic intervention and reduce pleural-associated morbidity.
Topics: Cells, Cultured; Humans; Pleura; Pleural Neoplasms; Pleurisy; Pleurodesis; Tuberculosis, Pleural
PubMed: 9387973
DOI: 10.1183/09031936.97.10102411 -
Internal Medicine (Tokyo, Japan) Aug 1995A 51-year-old man was admitted to our hospital because of dry cough and low grade fever with right-sided pleural fluid and blood eosinophilia. Warfarin had been...
A 51-year-old man was admitted to our hospital because of dry cough and low grade fever with right-sided pleural fluid and blood eosinophilia. Warfarin had been prescribed following coronary artery bypass grafting. After the discontinuation of warfarin the clinical and chest X-ray findings improved; readministration of the drug caused recurrent blood eosinophilia and pleural effusion in the other lung. Since no other specific etiologies for eosinophilia and pleural effusion were determined by extensive evaluation, warfarin seemed to be associated with his illness. This is the first report of warfarin-induced eosinophilic pleurisy.
Topics: Anticoagulants; Eosinophilia; Humans; Male; Middle Aged; Pleurisy; Warfarin
PubMed: 8563124
DOI: 10.2169/internalmedicine.34.794 -
BMC Veterinary Research Aug 2018Pasteurella multocida type A (PmA) is considered a secondary agent of pneumonia in pigs. The role of PmA as a primary pathogen was investigated by challenging pigs with...
BACKGROUND
Pasteurella multocida type A (PmA) is considered a secondary agent of pneumonia in pigs. The role of PmA as a primary pathogen was investigated by challenging pigs with eight field strains isolated from pneumonia and serositis in six Brazilian states. Eight groups of eight pigs each were intranasally inoculated with different strains of PmA (1.5 mL/nostril of 10e7 CFU/mL). The control group (n = 12) received sterile PBS. The pigs were euthanized by electrocution and necropsied by 5 dpi. Macroscopic lesions were recorded, and swabs and fragments of thoracic and abdominal organs were analyzed by bacteriological and pathological assays. The PmA strains were analyzed for four virulence genes (toxA: toxin; pfhA: adhesion; tbpA and hgbB: iron acquisition) by PCR and sequencing and submitted to multilocus sequence typing (MLST).
RESULTS
The eight PmA strains were classified as follows: five as highly pathogenic (HP) for causing necrotic bronchopneumonia and diffuse fibrinous pleuritis and pericarditis; one as low pathogenic for causing only focal bronchopneumonia; and two as nonpathogenic because they did not cause injury to any pig. PCR for the gene pfhA was positive for all five HP isolates. Sequencing demonstrated that the pfhA region of the HP strains comprised four genes: tpsB1, pfhA1, tpsB2 and pfhA2. The low and nonpathogenic strains did not contain the genes tpsB2 and pfhA2. A deletion of four bases was observed in the pfhA gene in the low pathogenic strain, and an insertion of 37 kb of phage DNA was observed in the nonpathogenic strains. MLST clustered the HP isolates in one group and the low and nonpathogenic isolates in another. Only the nonpathogenic isolates matched sequence type 10; the other isolates did not match any type available in the MLST database.
CONCLUSIONS
The hypothesis that some PmA strains are primary pathogens and cause disease in pigs without any co-factor was confirmed. The pfhA region, comprising the genes tpsB1, tpsB2, pfhA1 and pfhA2, is related to the pathogenicity of PmA. The HP strains can cause necrotic bronchopneumonia, fibrinous pleuritis and pericarditis in pigs and can be identified by PCR amplification of the gene pfhA2.
Topics: Animals; Brazil; Bronchopneumonia; Genes, Bacterial; Multilocus Sequence Typing; Pasteurella Infections; Pasteurella multocida; Pericarditis; Pleurisy; Polymerase Chain Reaction; Swine; Swine Diseases; Virulence
PubMed: 30134904
DOI: 10.1186/s12917-018-1565-2 -
American Journal of Respiratory Cell... Apr 2021is the leading cause of hospital community-acquired pneumonia. Patients with pneumococcal pneumonia may develop complicated parapneumonic effusions or empyema that can...
is the leading cause of hospital community-acquired pneumonia. Patients with pneumococcal pneumonia may develop complicated parapneumonic effusions or empyema that can lead to pleural organization and subsequent fibrosis. The pathogenesis of pleural organization and scarification involves complex interactions between the components of the immune system, coagulation, and fibrinolysis. EPCR (endothelial protein C receptor) is a critical component of the protein C anticoagulant pathway. The present study was performed to evaluate the role of EPCR in the pathogenesis of infection-induced pleural thickening and fibrosis. Our studies show that the pleural mesothelium expresses EPCR. Intrapleural instillation of impairs lung compliance and lung volume in wild-type and EPCR-overexpressing mice but not in EPCR-deficient mice. Intrapleural infection induces pleural thickening in wild-type mice. Pleural thickening is more pronounced in EPCR-overexpressing mice, whereas it is reduced in EPCR-deficient mice. Markers of mesomesenchymal transition are increased in the visceral pleura of infected wild-type and EPCR-overexpressing mice but not in EPCR-deficient mice. The lungs of wild-type and EPCR-overexpressing mice administered intrapleural showed increased infiltration of macrophages and neutrophils, which was significantly reduced in EPCR-deficient mice. An analysis of bacterial burden in the pleural lavage, the lungs, and blood revealed a significantly lower bacterial burden in EPCR-deficient mice compared with wild-type and EPCR-overexpressing mice. Overall, our data provide strong evidence that EPCR deficiency protects against infection-induced impairment of lung function and pleural remodeling.
Topics: Animals; Bacterial Load; Cells, Cultured; Disease Models, Animal; Endothelial Protein C Receptor; Female; Fibrosis; Host-Pathogen Interactions; Humans; Lung; Macrophages; Male; Mice, Inbred C57BL; Mice, Knockout; Neutrophil Infiltration; Neutrophils; Pleura; Pleural Effusion; Pleurisy; Pneumonia, Pneumococcal; Streptococcus pneumoniae; Mice
PubMed: 33600743
DOI: 10.1165/rcmb.2020-0328OC -
Journal of Ethnopharmacology Jun 2016The leaves and stems bark of Memora nodosa (Silva Manso) Miers (Bignoniaceae) are used in Brazilian traditional medicine in the treatment of external ulcers and wounds;...
ETHNOPHARMACOLOGICAL RELEVANCE
The leaves and stems bark of Memora nodosa (Silva Manso) Miers (Bignoniaceae) are used in Brazilian traditional medicine in the treatment of external ulcers and wounds; its roots are used to treat abdominal pain and scabies.
AIM OF THE STUDY
Our aim was to evaluate the antinociceptive and anti-inflammatory activities of Memora nodosa roots ethanolic extract (EMN) and allantoin, a secondary metabolite isolated from this plant.
MATERIALS AND METHODS
The EMN and allantoin antinociceptive activity were evaluated in mice using both chemical and heat-induced pain models such as acetic acid-induced writhing, formalin and tail-flick tests. In the formalin test, a pre-treatment with naloxone was used to verify an involvement of opioid receptor in the antinociceptive effect of EMN and allantoin. Pre-treatment with glibenclemide was used to verity an involvement of ATP-sensitive K(+)channel in the allantoin antinociceptive effect. EMN and allantoin anti-inflammatory activity were assessed by carrageenan-induced paw edema and pleurisy tests.
RESULTS
The treatment with EMN (250, 500 and 1000mg/kg, p.o.) inhibit the acetic acid and formalin (both phases)-induced nociception. However, just at doses 500 and 1000mg/kg increased the latency time in tail-flick test. These results suggest the involvement of both peripheral and central antinociceptive mechanisms. The treatment with allantoin (40, 60 and 80mg/kg p.o.) produced a dose-dependent antinociceptive effect in both phases of formalin-induced nociception test; allantoin (60mg/kg) was not able to increase the latency time in tail flick-test. The pre-treatment with naloxone completely reversed the EMN (1000mg/kg) and allantoin (60mg/kg) effect in the first phase of formalin test; and glibenclamide reversed the allantoin effect. The administration of EMN (250, 500 and 1000mg/kg) and allantoin (60mg/kg) showed significant anti-inflammatory activity in the whole carrageenan-induced paw edema. Furthermore, EMN and allantoin reduced the leukocytes migration and pleural exudate to the pleural cavity.
CONCLUSION
EMN have significant antinociceptive and anti-inflammatory effects, which appear to be, at least in part, due to the presence of allantoin. However, allantoin is not responsible for the EMN central antinociceptive activity. Allantoin has peripheral antinociceptive activity that involves the opioid receptor and ATP-sensitive K(+)channels. Opioid receptors are also involved in the EMN antinociceptive activity. These findings support the use of Memora nodosa in popular medicine and demonstrate that this plant has therapeutic potential for the development of antinociceptive and anti-inflammatory phytomedicines.
Topics: Acetic Acid; Allantoin; Analgesics; Animals; Anti-Inflammatory Agents; Bignoniaceae; Carrageenan; Edema; Formaldehyde; KATP Channels; Male; Mice; Pain; Phytotherapy; Plant Extracts; Plant Roots; Pleurisy; Receptors, Opioid
PubMed: 27079223
DOI: 10.1016/j.jep.2016.04.010 -
Acta Gastro-enterologica Belgica 2018Cytomegalovirus (CMV) reactivation is a common complication after liver transplantation. In patients with CMV infection, indicated by a positive CMV DNA titer, the...
Cytomegalovirus (CMV) reactivation is a common complication after liver transplantation. In patients with CMV infection, indicated by a positive CMV DNA titer, the presence of any clinical symptom is termed CMV disease. The most common organ affected in CMV disease is the gastrointestinal tract, causing esophagitis, gastritis, enteritis or colitis. CMV infection of the pleura and pericard has been reported in immunocompromised patients, but is rarely seen following liver transplantation.We report a case of a 59-year-old male who developed CMV pleuropericarditis after liver transplantation. Initial ganciclovir treatment did not improve the patient's symptoms and therapy was switched to Foscarnet which ultimately resulted in resolution of infection. However, a few weeks after Foscarnet cessation, the patient again developed bilateral pleural effusion. Ultimate biochemical and clinical response was achieved with IV ganciclovir treatment. The patient was discharged from the hospital with oral Valganciclovir for 3 weeks and has since remained relapse free for >1 year.
Topics: Antiviral Agents; Cytomegalovirus Infections; Drainage; Ganciclovir; Graft Rejection; Humans; Immunosuppressive Agents; Liver Cirrhosis, Alcoholic; Liver Transplantation; Male; Middle Aged; Pericardiocentesis; Pericarditis; Pleurisy; Thoracentesis; Tomography, X-Ray Computed
PubMed: 30350533
DOI: No ID Found -
Tuberkuloz Ve Toraks Sep 2020In recent years, there have been a significant increase in the tests and biomarkers available for pleural fluid analysis. YKL-40 is one of the inflammatory biomarkers... (Observational Study)
Observational Study
INTRODUCTION
In recent years, there have been a significant increase in the tests and biomarkers available for pleural fluid analysis. YKL-40 is one of the inflammatory biomarkers that is used for this purpose. The aim of our study is to assess the levels and diagnostic values of YKL-40 in patients with different types of pleural effusions (PE).
MATERIALS AND METHODS
This was a prospective, observational and crosssectional study. Pleural and serum YKL-40 levels were measured using enzyme-linked immunosorbent assay in 119 patients with PEs, including 23 transudates PE, 47 malignant PE, 26 parapneumonic PE (PPPE), 17 paramalignant PE (PME) and 6 tuberculous PE (TBPE).
RESULT
Median pleural YKL-40 level was higher in exudates (390.3 ng/mL) than in transudates (369.5 ng/mL) (p<0.02). For a cut-off level of 378 ng/mL, it was found to predict exudates with 70% sensitivity and 64% specificity. [area under the curve (AUC)= 0.660, p= 0.01]. Median pleural YKL-40 level was highest in PMEs (407.1 ng/mL) and the lowest in transudates (369.5 ng/ mL) and high levels, with a cut-off value of 396 ng/mL, differentiated PMEs from other subgroups with 65% sensitivity and 68% specificity. (AUC= 0.680, p= 0.02). Median serum YKL-40 level was the highest in PPPEs (351.4 ng/mL) and the lowest in TBPEs (114.2 ng/mL) (p= 0.01). For a cut-off level of 284 ng/mL, it differentiated PPPEs from TBPEs with 61% sensitivity and 100% specificity (AUC= 0.830, p= 0.01). In TBPEs, pleural/serum YKL-40 ratio was strongly related with pleural ADA (r= 1, p= 0.04).
CONCLUSIONS
Pleural YKL-40 may be useful for differentiating exudates and detecting PMEs. Serum YKL-40 may be good diagnostic biomarker for differentiating PPPEs and TBPEs. Additionally, measuring serum and pleural YKL-40 and pleural ADA may be reliable way to diagnose TBPEs.
Topics: Adult; Aged; Biomarkers; Chitinase-3-Like Protein 1; Cross-Sectional Studies; Exudates and Transudates; Female; Humans; Male; Middle Aged; Pleural Effusion; Pleurisy; Prospective Studies
PubMed: 33295725
DOI: 10.5578/tt.70090