scholarly journals Biochemistry in Assessing the Inflammatory Response of the Respiratory System Due to Experimental Exposure to Glass Fibres

2019 ◽  
Vol 56 (1) ◽  
pp. 285-290
Author(s):  
Bianca Domokos-Hancu ◽  
Milena Adina Man ◽  
Antigona Carmen Trofor ◽  
Carmen Monica Pop ◽  
Cristina Maria Gavrilescu ◽  
...  

Given the structural resemblances between glass fiber and asbestos, it is important to understand the mechanisms through which exposure to glass fibers may affect the respiratory system. To study the effect of glass fiber on rat lung through intratracheal exposure, considering the subject�s weight variation, together with haematological parameters, C-reactive protein (CRP), total number of lymphocytes, and IL8 concentration in bronchoalveolar lavage. We performed an intratracheal instillation study on four groups of 8 randomly selected Wistar rats, by administering 3 different doses of glass fiber. The hematocrit value was an indirect indicator of chronic hypoxemia; leukocytes and the C-reactive protein assessed systemic inflammation, and total number of lymphocytes and IL8 concentration in bronchoalveolar lavage fluid determined the lung�s inflammatory response. Weight variation evaluated in all 8 measurements revealed no statistically significant changes (p=0.768). The decrease in mean blood leukocytes was interpreted in relation with the glass fiber dose, with a statistically significant difference between the study groups (p=0.003). Statistically significant differences were found in the CRP values, with dose correlations (p[0.001). The bronchoalveolar lavage fluid showed increased levels of IL-8 (p[0.05), and decrease of lymphocytes (p[0.001) in correlation with the administered glass fiber dose. The inflammatory response following exposure to glass fibers in rats is correlated with administrated glass fiber dose. The alterations described as a result of intratracheal glass fiber instillation could predict the effects which occupational exposure to glass fiber may produce in humans.

2009 ◽  
Vol 41 (8) ◽  
pp. 3409-3413 ◽  
Author(s):  
R. Vos ◽  
B.M. Vanaudenaerde ◽  
S.I. De Vleeschauwer ◽  
A. Willems-Widyastuti ◽  
L.J. Dupont ◽  
...  

Allergy ◽  
1989 ◽  
Vol 44 (2) ◽  
pp. 98-102 ◽  
Author(s):  
M. Söderberg ◽  
R. Lundgren ◽  
L. Bjermer ◽  
N. Stjernberg ◽  
L. Rosenhall

2010 ◽  
pp. 937-944
Author(s):  
P Dostál ◽  
M Šenkeřík ◽  
R Pařízková ◽  
D Bareš ◽  
P Živný ◽  
...  

Hypothermia was shown to attenuate ventilator-induced lung injury due to large tidal volumes. It is unclear if the protective effect of hypothermia is maintained under less injurious mechanical ventilation in animals without previous lung injury. Tracheostomized rats were randomly allocated to non-ventilated group (group C) or ventilated groups of normothermia (group N) and mild hypothermia (group H). After two hours of mechanical ventilation with inspiratory fraction of oxygen 1.0, respiratory rate 60 min-1, tidal volume 10 ml·kg-1, positive end-expiratory pressure (PEEP) 2 cm H2O or immediately after tracheostomy in non-ventilated animals inspiratory pressures were recorded, rats were sacrificed, pressure-volume (PV) curve of respiratory system constructed, bronchoalveolar lavage (BAL) fluid and aortic blood samples obtained. Group N animals exhibited a higher rise in peak inspiratory pressures in comparison to group H animals. Shift of the PV curve to right, higher total protein and interleukin6 levels in BAL fluid were observed in normothermia animals in comparison with hypothermia animals and non-ventilated controls. Tumor necrosis factor-α was lower in the hypothermia group in comparison with normothermia and non-ventilated groups. Mild hypothermia attenuated changes in respiratory system mechanics and modified cytokine concentration in bronchoalveolar lavage fluid during low lung volume ventilation in animals without previous lung injury.


2019 ◽  
Vol 57 (10) ◽  
pp. 1632-1637 ◽  
Author(s):  
Akihiro Ito ◽  
Tadashi Ishida ◽  
Hiromasa Tachibana ◽  
Machiko Arita ◽  
Akio Yamazaki ◽  
...  

Abstract Background This study aimed to investigate the usefulness of inflammatory biomarkers such as white blood cell (WBC) count, C-reactive protein (CRP) and procalcitonin (PCT) for differentiating cryptogenic organising pneumonia (COP) from community-acquired pneumonia (CAP). Methods COP patients hospitalised in Kurashiki Central Hospital between January 2010 and December 2017 whose WBC counts and CRP and PCT levels were measured were investigated retrospectively, and their results were compared with those of hospitalised CAP patients who were prospectively enrolled between October 2010 and November 2017. Definite COP was defined by specific histopathological findings, and possible COP was defined as a consolidation shadow on chest computed tomography and lymphocyte dominance in bronchoalveolar lavage fluid in the absence of specific histopathological findings or lung specimens. The discriminatory abilities of WBC counts, CRP and PCT were evaluated by receiver operating characteristic (ROC) curve analysis. Results There were 56 patients in the entire COP group, 35 (61.4%) with definite COP, and 914 CAP patients. All three biomarkers were significantly lower in COP than in CAP. The AUC value of PCT in all COP patients was 0.79, significantly higher than of both CRP (AUC 0.59, p < 0.001) and WBC (AUC 0.69, p = 0.048). In definite COP patients, the AUC value of PCT was 0.79, which was also significantly higher than of both WBC (AUC 0.64, p = 0.006) and CRP (AUC 0.64, p = 0.001). Conclusions PCT is a more useful biomarker for differentiating COP from CAP than WBC count or CRP. However, PCT should be used as an adjunct to clinical presentation and radiological findings.


2007 ◽  
Vol 53 (10) ◽  
pp. 1782-1791 ◽  
Author(s):  
Brendan J McMorran ◽  
Severine A Ouvry Patat ◽  
John B Carlin ◽  
Keith Grimwood ◽  
Alun Jones ◽  
...  

Abstract Background: Airway inflammation in cystic fibrosis (CF) is exaggerated and characterized by neutrophil-mediated tissue destruction, but its genesis and mechanisms remain poorly understood. To further define the pulmonary inflammatory response, we conducted a proteome-based screen of bronchoalveolar lavage fluid (BALF) collected from young children with and without CF experiencing endobronchial infection. Methods: We collected BALF samples from 45 children younger than 5 years and grouped them according to the presence of respiratory pathogens: ≥1 × 105 colony-forming units (CFU)/mL BALF (18 and 12 samples with and without CF, respectively) and &lt;1 × 105 CFU/mL (23 and 15 samples). BALF proteins were analyzed with SELDI-TOF mass spectrometry (MS) and H4 ProteinChips®. Proteins were identified and characterized using trypsin digestion, tandem MS, Fourier transform ion cyclotron resonance MS, immunoblotting, and ELISA. Results: The SELDI-TOF MS BALF profiles contained 53 unique, reliably detected proteins. Peak intensities of 24 proteins differed significantly between the CF and non-CF samples. They included the neutrophil proteins, α-defensin 1 and 2, S100A8, S100A9, and S100A12, as well as novel forms of S100A8 and S100A12 with equivalent C-terminal deletions. Peak intensities of these neutrophil proteins and immunoreactive concentrations of selected examples were significantly higher in CF than non-CF samples. Conclusions: Small neutrophil-derived BALF proteins, including novel C-terminal truncated forms of S100A proteins, are easily detected with SELDI-TOF MS. Concentrations of these molecules are abnormally high in early CF lung disease. The data provide new insights into CF lung disease and identify novel proteins strongly associated with CF airway inflammation.


2004 ◽  
Vol 286 (3) ◽  
pp. L488-L493 ◽  
Author(s):  
Michael A. Vozzelli ◽  
S. Nicholas Mason ◽  
Mary H. Whorton ◽  
Richard L. Auten

Macrophage-derived cytokines may provoke the inflammatory response in lung injury. Because macrophage influx is a prominent feature of the cellular inflammatory response accompanying the development of bronchopulmonary dysplasia, we hypothesized that blocking macrophage influx would reduce overall cellular influx and oxidative damage. Newborn rats were exposed at birth to 95% O2or air for 1 wk, and hyperoxia-exposed pups were injected with anti-monocyte chemoattractant protein-1 (MCP-1) or IgG control on days 3–5. MCP-1 was increased in bronchoalveolar lavage fluid and in histological sections from the 95% O2-exposed, IgG-injected pups compared with air-exposed controls. At 1 wk, anti-MCP-1-treated pups had reduced leukocyte numbers, both macrophages and neutrophils, in bronchoalveolar lavage fluid compared with IgG-treated controls. Cytokine-induced neutrophil chemoattractant-1, the rat analog of IL-8, was not significantly decreased in lavage fluid but was reduced in lung cells in anti-MCP-1-treated pups. Tissue carbonyls, a measure of protein oxidation, were decreased in anti-MCP-1-treated pups. Anti-MCP-1 treatment prevented neutrophil influx and reduced protein oxidation in hyperoxia-exposed newborn rats.


1997 ◽  
Vol 27 (4) ◽  
pp. 396-405 ◽  
Author(s):  
L. M. TERAN ◽  
M. G. CAMPOS ◽  
B. T. BEGISHVILLI ◽  
J.-M. SCHRODER ◽  
R. DJUKANOVIC ◽  
...  

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