Search

Objective: This study aims to evaluate the efficiencies and effects of different sclerosing agents. Materials and Methods: Thirty-five female Wistar-albino rats were included in this study and divided into five groups randomly. Isotonic saline (group 1), iodopovidone (group 2), rifamycin (group 3), autologous blood (group 4), talc (group 5) were given into intrapleural space. On postoperative 28th day, ipsilateral and contralateral pleural and parenchymal fibrosis and inflammation were evaluated. Results: There were statistically differences between control and other groups on macroscopically pleural fibrosis examination (p=0.004, p=0.001, p=0.001, p=0.000, respectively). Microscopically pleural fibrosis were determined in all groups when compared to control group (p=0.023, p=0.023, p=0.035, p=0.001, respectively). There were no significant differences between sclerosing agent groups (p>0.05). Significant differences were observed according to microscopic pleural inflammation evaluation between talc group and other groups. There was superiority in talc group according to intraparenchymal inflammation grade compared to other groups (p=0.010, p=0.042, p=0.030, respectively). Macroscopically, fibrosis and microscopically, inflammation were significantly observed between talc and other groups in the contralateral pleura (p = 0.037and p=0.009, respectively). Conclusion: Iodopovidone, autologous blood, talc, and rifamycin can be used as effective pleurodesis agents. However, we found that rifamycin and autologous blood are safer as effective pleurodesis agents. We think that these two agents can be used in patients with secondary lung diseases due to their less intraparenchymal inflammation rates. It may be advantageous to prefer other sclerosing agents which has lower costs and less side effects comparing to talc. [ABSTRACT FROM AUTHOR]

Carbon nanotubes (CNTs) are speculated to cause mesothelioma by persistent inflammation, oxidative stress, tissue injury, and genotoxicity. To investigate the pleural response to CNTs, we exposed C57BL/6 mice by intrapleural injection of 0.2 or 5 µg multiwalled CNTs (MWCNT-7, NM-401, and NM-403) or single-walled CNTs (NM-411). Inflammatory response, cellular reactive oxygen species (ROS) production of pleural lavage cells, and genotoxicity in cells from the mesothelial surface were assessed at days 1 and 90 after the exposure. Long and rigid types of MWCNTs (MWCNT-7 and NM-401) caused acute inflammation, characterized by influx of macrophages, neutrophils, and eosinophils into the pleural cavity. The inflammation was still evident at 90 days after the exposure, although it had reduced dramatically. The cellular ROS production was increased at day 90 after the exposure to MWCNT-7 and NM-401. The short and tangled type of MWCNT (ie NM-403) did not cause pleural inflammation or ROS production in pleural fluid cells. The exposure to NM-411 did not cause consistent inflammation responses or cellular ROS production. Levels of DNA strand breaks and DNA oxidation damage were unaltered, except for NM-411-exposed mice that had increased levels of DNA strand breaks at 90 days after the exposure. In conclusion, the long and rigid CNTs caused prolonged inflammatory response and increased ROS production in pleural lavage cells, yet it was not reflected in higher levels of DNA damage in pleural tissue. [ABSTRACT FROM AUTHOR]

This study investigated the antiinflammatory properties of betulinic acid (BA) and xylopic acid (XA) extracted from Margaritaria discoidea and Xylopia aethiopica, respectively. M. discoidea and X. aethiopica are plants native in Ghana and the West-African region and used traditionally to treat different pathologies including inflammatory conditions. The antiinflammatory effect of BA and XA was established by an in vivo assay using the carrageenan-induced pleural inflammation model in mice. Also, the ability of BA and XA to increase catalase, superoxide dismutase, glutathione levels and decrease lipid peroxidation level in reactive oxidative assays was assessed. In addition, the ability of XA and BA to prevent potential lung tissue damage was quantified. Pretreatment with BA and XA reduced significantly, signs of inflammation: neutrophil infiltration, oedema, and alveoli septal thickening in carrageenan-treated lung tissue. Additionally, BA or XA pretreatment lowered the degree of lipid peroxidation in the lung tissue while increasing the levels of catalase, superoxide dismutase, and glutathione in vivo. Comparatively, XA was more efficacious than BA in the prevention of lung tissue damage. BA and XA derived from X. aethiopica and M. discoidea possess antiinflammatory and in vivo antioxidant activities in mice pleurisy model. The effect of these compounds gives credence to the traditional use in the management of inflammatory conditions of the airway. [ABSTRACT FROM AUTHOR]

ABSTRACT Background and objective Exudative pleural effusions affect over 1500 patients per million population each year. The pathobiology of pleural exudate formation remains unclear. Our recent study revealed monocyte chemotactic protein-1 ( MCP-1) as a key driver of fibrinolytic-induced exudate effusion while another study found a role for MCP-1 in malignant effusion formation. In the present study, we further evaluated the role of MCP-1 in the development of pleural effusion in a mouse model of acute pleural inflammation. Methods λ-Carrageenan ( CAR) was injected into the pleural cavity of CD1 mice and pleural effusion volume measured up to 16 h post-injection. Pleural effusion and serum protein and MCP-1 concentrations were measured and differential cell counts performed in fluids. Mice were also treated with either intraperitoneal (i) anti- MCP-1 antibody or isotype control or (ii) an MCP-1 receptor ( CCR2) antagonist or vehicle control 12 h prior to and at the time of CAR injection. Results Intrapleural CAR induced significant pleural fluid accumulation (300.0 ± 49.9 μL) in mice after 4 h. Pleural fluid MCP-1 concentrations were significantly higher than corresponding serum MCP-1 (144 603 ± 23 204 pg/ mL vs 3703 ± 801 pg/ mL, P < 0.0001). A significant decrease in pleural fluid formation was seen both with anti- MCP-1 antibody (median (interquartile range, IQR): 36 (0-168) μL vs controls 290 (70-436) μL; P = 0.02) or CCR2 antagonist (153 (30-222) μL vs controls 240 (151-331) μL, P = 0.0049). Conclusions Blockade of MCP-1 activity significantly reduced inflammatory pleural effusion formation in a CAR model. Together with recent successes in MCP-1 blockade in other effusion formation models, our data strongly support clinical evaluation of MCP-1 antagonists as a novel approach to pleural fluid management. [ABSTRACT FROM AUTHOR]

Multiwalled carbon nanotubes ( MWCNT) have a fibrous structure similar to asbestos, raising concern that MWCNT exposure may lead to asbestos-like diseases. Previously we showed that MWCNT translocated from the lung alveoli into the pleural cavity and caused mesothelial proliferation and fibrosis in the visceral pleura. Multiwalled carbon nanotubes were not found in the parietal pleura, the initial site of development of asbestos-caused pleural diseases in humans, probably due to the short exposure period of the study. In the present study, we extended the exposure period to 24 weeks to determine whether the size and shape of MWCNT impact on deposition and lesion development in the pleura and lung. Two different MWCNTs were chosen for this study: a larger sized needle-like MWCNT ( MWCNT- L; l = 8 μm, d = 150 nm), and a smaller sized MWCNT ( MWCNT- S; l = 3 μm, d = 15 nm), which forms cotton candy-like aggregates. Both MWCNT- L and MWCNT- S suspensions were administered to the rat lung once every 2 weeks for 24 weeks by transtracheal intrapulmonary spraying. It was found that MWCNT- L, but not MWCNT- S, translocated into the pleural cavity, deposited in the parietal pleura, and induced fibrosis and patchy parietal mesothelial proliferation lesions. In addition, MWCNT- L induced stronger inflammatory reactions including increased inflammatory cell number and cytokine/chemokine levels in the pleural cavity lavage than MWCNT- S. In contrast, MWCNT- S induced stronger inflammation and higher 8-hydroxydeoxyguanosine level in the lung tissue than MWCNT- L. These results suggest that MWCNT- L has higher risk of causing asbestos-like pleural lesions relevant to mesothelioma development. [ABSTRACT FROM AUTHOR]

The FDG-PET (fluorine-18 fluorodeoxyglucose positron emission tomography) scan is used with increasing frequency to investigate pleural abnormalities and to determine the possibility of neoplastic invasion. However, false-positive findings are not uncommon and talc pleurodesis has been reported to cause hypermetabolic pleural thickenings up to 5 years after the procedure. We report the cases of 3 patients (2 of whom had a history of asbestos exposure) requiring talc pleurodesis for recurrent pneumothoraces between 1988 and 1990, who were investigated in 2011 for pleural abnormalities. Avid pleural thickening on FDG-PET scan mimicking pleural cancer was found, but this was deemed secondary to the pleurodesis. Talc pleurodesis generates inflammation which promotes pleural adhesions. This inflammatory reaction could decrease with time, as in other inflammatory processes. Since talc is not metabolized by the body, the FDG-PET scan can remain positive, most likely because of a foreign-body granulomatous reaction, even 20 years later. It is important to be aware of this possibility and to question patients with pleural abnormalities about past procedures and mention such procedures to the colleagues who are responsible for interpreting metabolic imaging. Follow-up of hypermetabolic pleural lesions attributed to talc pleurodesis is important for the detection of new pleural lesions or neoplastic evolution. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Suspicion has been raised that high aspect ratio nanoparticles or nanofibers might possess asbestos-like pathogenicity. The pleural space is a specific target for disease in individuals exposed to asbestos and by implication of nanofibers. Pleural effects of fibers depends on fiber length, but the key threshold length beyond which adverse effects occur has never been identified till now because all asbestos and vitreous fiber samples are heterogeneously distributed in their length. Nanotechnology advantageously allows for highly defined length distribution of synthetically engineered fibers that enable for in-depth investigation of this threshold length. We utilized the ability to prepare silver nanofibers of five defined length classes to demonstrate a threshold fiber length for acute pleural inflammation. Nickel nanofibers and carbon nanotubes were then used to strengthen the relationship between fiber length and pleural inflammation. A method of intrapleural injection of nanofibers in female C57Bl/6 strain mice was used to deliver the fiber dose, and we then assessed the acute pleural inflammatory response. Chest wall sections were examined by light and scanning electron microscopy to identify areas of lesion; furthermore, cell- nanowires interaction on the mesothelial surface of the parietal pleura in vivo was investigated. Our results showed a clear threshold effect, demonstrating that fibers beyond 4 µm in length are pathogenic to the pleura. The identification of the threshold length for nanofiber-induced pathogenicity in the pleura has important implications for understanding the structure-toxicity relationship for asbestos-induced mesothelioma and consequent risk assessment with the aim to contribute to the engineering of synthetic nanofibers by the adoption of a benign-by-design approach. [ABSTRACT FROM AUTHOR]