Antimacrophage chemokine treatment prevents neutrophil and macrophage influx in hyperoxia-exposed newborn rat lung

2004 ◽  
Vol 286 (3) ◽  
pp. L488-L493 ◽  
Author(s):  
Michael A. Vozzelli ◽  
S. Nicholas Mason ◽  
Mary H. Whorton ◽  
Richard L. Auten
Keyword(s):  
Inflammatory Response ◽  
Bronchoalveolar Lavage ◽  
Protein Oxidation ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Lung Cells ◽  
Newborn Rats ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Cellular Inflammatory Response

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.

Inflammatory response in bronchoalveolar lavage fluid after inhaling histamine

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

Effects of electronic cigarette aerosol on isolated murine lung cells and bronchoalveolar lavage fluid

2018 ◽  
Author(s):  
Elsa Tadele Roxlau ◽  
Alexandra Pichl ◽  
Balachandar Selvakumar ◽  
Ralph T. Schermuly ◽  
Hossein A. Ghofrani ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Electronic Cigarette ◽  
Lung Cells ◽  
Murine Lung

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 ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Bronchoalveolar Lavage ◽  
Glass Fiber ◽  
Respiratory System ◽  
Bronchoalveolar Lavage Fluid ◽  
Glass Fibers ◽  
Lavage Fluid ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Weight Variation

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.

Leukotrienes mediate part of Ova-induced lung effects in mice via EGFR

2003 ◽  
Vol 285 (4) ◽  
pp. L808-L818 ◽  
Author(s):  
B. Boris Vargaftig ◽  
Monique Singer
Keyword(s):  
Bronchoalveolar Lavage Fluid ◽  
Egf Receptor ◽  
Kinase Inhibitor ◽  
Airway Remodeling ◽  
Intratracheal Instillation ◽  
Lavage Fluid ◽  
Egfr Tyrosine Kinase Inhibitor ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Cysteinyl Leukotriene

Antigen induces murine bronchial hyperreactivity (BHR), inflammation, mucus accumulation, and airway remodeling. To investigate whether leukotrienes (LT) mediate the effects of antigen [ovalbumin (Ova)], we studied 5-lipoxygenase (5-LO) expression in immunized BP2 mice and blocked LT synthesis with the 5-LO inhibitor zileuton or antagonized their effects with receptor antagonists [cysteinyl leukotriene (Cys-LT)-ra MK-571, LY-171883; LTB4-ra PH-163]. Cys-LT content increased in the bronchoalveolar lavage fluid (BALF) as early as 15 min after the intratracheal instillation of Ova. Zileuton inhibited LT release in the BALF and eosinophil recruitment in the lungs, and dose dependently reduced BHR, mucus accumulation, and remodeling, as did the LT-ra. Thus LT, released just after antigen challenge, might constitute the first step in accounting for the effects of Ova. Because mucus accumulation is regulated via the EGF receptor (EGFR), which is also implicated in the effects of LT, we studied this pathway with AG-1478, an EGFR tyrosine kinase inhibitor given at 0.5, 4, and 20 mg/kg. AG-1478 inhibited BHR, inflammation, and lung remodeling induced by Ova or by molecules themselves generated by Ova, such as LT, IL-13, and monocyte chemoattractant protein-1, which promote identical effects, suggesting the involvement of the EGFR pathway in the asthma-like syndrome observed.

Leukotrienes, IL-13, and chemokines cooperate to induce BHR and mucus in allergic mouse lungs

2003 ◽  
Vol 284 (2) ◽  
pp. L260-L269 ◽  
Author(s):  
B. Boris Vargaftig ◽  
Monique Singer
Keyword(s):  
Bronchoalveolar Lavage ◽  
Positive Feedback ◽  
Lung Inflammation ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Lipoxygenase Inhibitor ◽  
Monocyte Chemoattractant ◽  
Independent Events ◽  
Mouse Lungs ◽  
Allergic Mouse

In mice, intratracheal challenges with antigen (ovalbumin) or recombinant murine interleukin-13 (IL-13) induce lung inflammation, bronchial hyperreactivity (BHR), and mucus accumulation as independent events (Singer M, Lefort J, and Vargaftig BB. Am J Respir Cell Mol Biol 26: 74–84, 2002), largely mediated by leukotrienes (LT). We previously showed that LTC4 was released 15 min after ovalbumin, and we show that it induces the expression of monocyte chemoattractant proteins 1 and 5 and KC in the lungs, as well as IL-13 mRNA. Instilled intratracheally, these chemokines induced BHR and mucus accumulation, which were inhibited by the 5-lipoxygenase inhibitor zileuton and by the cysteinyl-LT receptor antagonist MK-571, suggesting mediation by cysteinyl-LT. Because these chemokines also induced release of LT into the bronchoalveolar lavage fluid and IL-13 into the lungs, we hypothesize that LT- and chemokine-based loops for positive-feedback regulations cooperate to maintain and amplify BHR and lung mucus accumulation after allergic challenge and in situations where IL-13, LT, or chemokines are generated.

scholarly journals Novel Neutrophil-Derived Proteins in Bronchoalveolar Lavage Fluid Indicate an Exaggerated Inflammatory Response in Pediatric Cystic Fibrosis Patients

2007 ◽  
Vol 53 (10) ◽  
pp. 1782-1791 ◽  
Author(s):  
Brendan J McMorran ◽  
Severine A Ouvry Patat ◽  
John B Carlin ◽  
Keith Grimwood ◽  
Alun Jones ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Inflammatory Response ◽  
Bronchoalveolar Lavage ◽  
Lung Disease ◽  
Airway Inflammation ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Respiratory Pathogens ◽  
Tissue Destruction ◽  
Tof Ms

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 <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.

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