Comparison of metabolites in exhaled breath and bronchoalveolar lavage fluid samples in a mouse model of asthma

2011 ◽  
Vol 111 (4) ◽  
pp. 1088-1095 ◽  
Author(s):  
Stephanie Neuhaus ◽  
Luzia Seifert ◽  
Wolfgang Vautz ◽  
Jürgen Nolte ◽  
Albrecht Bufe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Bronchoalveolar Lavage Fluid ◽  
Allergic Airway Inflammation ◽  
Lavage Fluid ◽  
Exhaled Breath ◽  
Ion Mobility Spectrometer ◽  
Eosinophilic Granulocytes

Background: A multi-capillary column ion mobility spectrometer (MCC/IMS) was developed to provide a method for the noninvasive diagnosis of lung diseases. The possibility of measuring the exhaled breath of mice was evaluated previously. The aim of the present study was to reveal whether mice affected by airway inflammation can be identified via MCC/IMS. Methods: Ten mice were sensitized and challenged with ovalbumin to induce allergic airway inflammation. The breath and volatile compounds of bronchoalveolar lavage fluid (BALF) were measured by MCC/IMS. Furthermore, histamine, nitric oxide, and arachidonic acid were determined as inflammatory markers in vitro. Results: Six volatile molecules were found in the BALF headspace at a significantly higher concentration in mice with airway inflammation compared with healthy animals. The concentration of substances correlated with the numbers of infiltrating eosinophilic granulocytes. However, substances showing a significantly different concentration in the BALF headspace were not found to be different in exhaled breath. Histamine and nitric oxide were identified by MCC/IMS in vitro but not in the BALF headspace or exhaled breath. Conclusion: Airway inflammation in mice is detectable by the analysis of the BALF headspace via MCC/IMS. Molecules detected in the BALF headspace of asthmatic mice at a higher concentration than in healthy animals may originate from oxidative stress induced by airway inflammation. As already described for humans, we found no correlation between the biomarker concentration in the BALF and the breath of mice. We suggest using the model described here to gain deeper insights into this discrepancy.

scholarly journals MTOR-Mediated Autophagy Is Involved in the Protective Effect of Ketamine on Allergic Airway Inflammation

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Hongyun Zou ◽  
Li-Xia Wang ◽  
Muzi Wang ◽  
Cheng Cheng ◽  
Shuai Li ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Protective Effect ◽  
Airway Inflammation ◽  
Bronchoalveolar Lavage Fluid ◽  
Mammalian Target Of Rapamycin ◽  
Allergic Airway Inflammation ◽  
Lavage Fluid ◽  
Morphological Findings ◽  
Airway Diseases ◽  
Inflammatory Mechanism

Unresolved inflammation underpins the pathogenesis of allergic airway diseases, such as asthma. Ketamine, accepted as a promising therapy for resistant asthma, has been demonstrated to attenuate allergic airway inflammation. However, the anti-inflammatory mechanism by ketamine in this setting is largely unknown. We aimed to investigate whether autophagy was involved in the protective effect of ketamine on allergic airway inflammation. Female C57BL/6 mice were sensitized to ovalbumin (OVA) and treated with ketamine at 25, 50, or 100 mg/kg prior to OVA challenge. In this model, the pulmonary morphological findings and airway inflammation were significantly inhibited at 50 mg/kg but not at 25 or 100 mg/kg. Moreover, 50 mg/kg ketamine abrogated the increased concentrations of inflammatory cytokines in bronchoalveolar lavage fluid (BALF) of allergic mice, as well as activated the expression of phosphorylated mammalian target of rapamycin (p-MTOR) and inhibited autophagy in allergic mice. To confirm whether the effect of 50 mg/kg ketamine on asthma was mediated by inhibiting autophagy, rapamycin was administered to mice sensitized to OVA and exposed to 50 mg/kg ketamine. All of the effect of 50 mg/kg ketamine was reversed by rapamycin treatment, including increased p-MTOR and decreased autophagy. Taken together, the present study demonstrates that 50 mg/kg ketamine inhibits allergic airway inflammation by suppressed autophagy, and this effect is mediated by the activation of MTOR in the lungs of allergic mice.

scholarly journals The Fermented Soy Product ImmuBalanceTM Suppresses Airway Inflammation in a Murine Model of Asthma

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3380
Author(s):  
Hideaki Kadotani ◽  
Kazuhisa Asai ◽  
Atsushi Miyamoto ◽  
Kohei Iwasaki ◽  
Takahiro Kawai ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Murine Model ◽  
Bronchoalveolar Lavage Fluid ◽  
Inflammatory Cell ◽  
Allergic Airway Inflammation ◽  
Lavage Fluid ◽  
Cell Infiltration ◽  
Mucus Production ◽  
Cell Counts

The fermented soy product ImmuBalance contains many active ingredients and its beneficial effects on some allergic diseases have been reported. We hypothesized that ImmuBalance could have potential effects on airway inflammation in a murine model of asthma. Mice sensitized and challenged with ovalbumin developed airway inflammation. Bronchoalveolar lavage fluid was assessed for inflammatory cell counts and levels of cytokines. Lung tissues were examined for cell infiltration and mucus hypersecretion. Oral administration of ImmuBalance significantly inhibited ovalbumin-induced eosinophilic inflammation and decreased Th2 cytokine levels in bronchoalveolar lavage fluid (p < 0.05). In addition, lung histological analysis showed that ImmuBalance inhibited inflammatory cell infiltration and airway mucus production. Our findings suggest that supplementation with ImmuBalance may provide a novel strategy for the prevention or treatment of allergic airway inflammation.

scholarly journals Adipose-Derived Stem Cells Ameliorate Allergic Airway Inflammation by Inducing Regulatory T Cells in a Mouse Model of Asthma

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Kyu-Sup Cho ◽  
Mi-Kyung Park ◽  
Shin-Ae Kang ◽  
Hee-Young Park ◽  
Sung-Lyong Hong ◽  
...  
Keyword(s):  
Stem Cells ◽  
T Cells ◽  
Regulatory T Cells ◽  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Bronchoalveolar Lavage Fluid ◽  
Immune Cell ◽  
Allergic Airway Inflammation ◽  
Lavage Fluid ◽  
Th2 Cytokines

Although several studies have demonstrated that mesenchymal stem cells derived from adipose tissue (ASCs) can ameliorate allergic airway inflammation, the immunomodulatory mechanism of ASCs remains unclear. In this study, we investigated whether regulatory T cells (Tregs) induction is a potential mechanism in immunomodulatory effects of ASCs on allergic airway disease and how these induced Tregs orchestrate allergic inflammation. Intravenous administration of ASCs significantly reduced allergic symptoms and inhibited eosinophilic inflammation. Airway hyperresponsiveness, total immune cell and eosinophils in the bronchoalveolar lavage fluid, mucus production, and serum allergen-specific IgE and IgG1 were significantly reduced after ASCs administration. ASCs significantly inhibited Th2 cytokines (IL-4, IL-5, and IL-13) and enhanced Th1 cytokine (IFN-γ) and regulatory cytokines (IL-10 and TGF-β) in the bronchoalveolar lavage fluid and lung draining lymph nodes. Furthermore, levels of IDO, TGF-β, and PGE2were significantly increased after ASCs administration. Interestingly, this upregulation was accompanied by increased Treg populations. In conclusion, ASCs ameliorated allergic airway inflammation and improved lung function through the induction of Treg expansion. The induction of Treg by ASCs involves the secretion of soluble factors such as IDO, TGF-β, and PGE2and Treg might be involved in the downregulation of Th2 cytokines and upregulation of Th1 cytokines production.

scholarly journals Cigarette smoke-induced necroptosis and DAMP release trigger neutrophilic airway inflammation in mice

2016 ◽  
Vol 310 (4) ◽  
pp. L377-L386 ◽  
Author(s):  
Simon D. Pouwels ◽  
G. Jan Zijlstra ◽  
Marco van der Toorn ◽  
Laura Hesse ◽  
Renee Gras ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Cigarette Smoke ◽  
Bronchoalveolar Lavage Fluid ◽  
Membrane Integrity ◽  
Lavage Fluid ◽  
Chronic Obstructive ◽  
Bronchial Epithelial ◽  
Proinflammatory Mediators

Recent data indicate a role for airway epithelial necroptosis, a regulated form of necrosis, and the associated release of damage-associated molecular patterns (DAMPs) in the development of chronic obstructive pulmonary disease (COPD). DAMPs can activate pattern recognition receptors (PRRs), triggering innate immune responses. We hypothesized that cigarette smoke (CS)-induced epithelial necroptosis and DAMP release initiate airway inflammation in COPD. Human bronchial epithelial BEAS-2B cells were exposed to cigarette smoke extract (CSE), and necrotic cell death (membrane integrity by propidium iodide staining) and DAMP release (i.e., double-stranded DNA, high-mobility group box 1, heat shock protein 70, mitochondrial DNA, ATP) were analyzed. Subsequently, BEAS-2B cells were exposed to DAMP-containing supernatant of CS-induced necrotic cells, and the release of proinflammatory mediators [C-X-C motif ligand 8 (CXCL-8), IL-6] was evaluated. Furthermore, mice were exposed to CS in the presence and absence of the necroptosis inhibitor necrostatin-1, and levels of DAMPs and inflammatory cell numbers were determined in bronchoalveolar lavage fluid. CSE induced a significant increase in the percentage of necrotic cells and DAMP release in BEAS-2B cells. Stimulation of BEAS-2B cells with supernatant of CS-induced necrotic cells induced a significant increase in the release of CXCL8 and IL-6, in a myeloid differentiation primary response gene 88-dependent fashion. In mice, exposure of CS increased the levels of DAMPs and numbers of neutrophils in bronchoalveolar lavage fluid, which was statistically reduced upon treatment with necrostatin-1. Together, we showed that CS exposure induces necrosis of bronchial epithelial cells and subsequent DAMP release in vitro, inducing the production of proinflammatory cytokines. In vivo, CS exposure induces neutrophilic airway inflammation that is sensitive to necroptosis inhibition.

Placebo-Controlled Study of Inhaled Budesonide on Indices of Airway Inflammation in Bronchoalveolar Lavage Fluid and Bronchial Biopsies in Cross-Country Skiers

Respiration ◽  
2000 ◽  
Vol 67 (4) ◽  
pp. 417-425 ◽  
Author(s):  
Malcolm Sue-Chu ◽  
Eeva-Maija Karjalainen ◽  
Annika Laitinen ◽  
Lars Larsson ◽  
Lauri A. Laitinen ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Controlled Study ◽  
Bronchial Biopsies ◽  
Cross Country ◽  
Inhaled Budesonide

A One Health Approach to Simple Liquid Sample Handling for Respiratory Based -Omics Analysis; Tracheal Wash and Bronchoalveolar Lavage Fluid

2021 ◽  
Author(s):  
Anna E. Karagianni ◽  
Samantha L. Eaton ◽  
Dominic Kurian ◽  
Eugenio Cillán-Garcia ◽  
Jonathan Twynam-Perkins ◽  
...  
Keyword(s):  
Respiratory Tract ◽  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Lower Respiratory Tract ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Lower Airway ◽  
Simple Liquid ◽  
Sample Handling ◽  
Sequential Screening

Abstract Airway inflammation is highly prevalent in horses, with the majority of non-infectious cases being defined as equine asthma. Currently, cytological analysis of airway derived samples is the principal method of assessing lower airway inflammation. Samples can be obtained by tracheal wash (TW) or by lavage of the lower respiratory tract (bronchoalveolar lavage fluid; BALF). Although BALF cytology carries significant diagnostic advantages over TW cytology, sample acquisition is invasive, making it prohibitive for routine and sequential-screening of airway health. The aim of this study was to establish a robust protocol to isolate macrophages, protein and RNA for molecular characterisation of TW samples and demonstrate the applicability of sample handling to rodent and human pediatric bronchoalveolar lavage fluid isolates. TW samples provided a good quality and yield of both RNA and protein for downstream transcriptomic/proteomic analyses. The sample handling methodologies were successfully applicable to BALF for rodent and human research. TW samples represent a rich source of airway cells, and molecular analysis to facilitate and study airway inflammation, based on both transcriptomic and proteomic analysis. This study provides a necessary methodological platform for future transcriptomic and/or proteomic studies on equine lower respiratory tract secretions and BALF samples from humans and mice.

Paeonol attenuates airway inflammation and hyperresponsiveness in a murine model of ovalbumin-induced asthma

2010 ◽  
Vol 88 (10) ◽  
pp. 1010-1016 ◽  
Author(s):  
Qiang Du ◽  
Gan-Zhu Feng ◽  
Li Shen ◽  
Jin Cui ◽  
Jian-Kang Cai
Keyword(s):  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Bronchoalveolar Lavage Fluid ◽  
Immunoglobulin E ◽  
Therapeutic Potential ◽  
Lavage Fluid ◽  
Interleukin 4 ◽  
Moutan Cortex ◽  
Ifn Γ ◽  
Anti Inflammatory

Paeonol, the main active component isolated from Moutan Cortex, possesses extensive pharmacological activities such as anti-inflammatory, anti-allergic, and immunoregulatory effects. In the present study, we examined the effects of paeonol on airway inflammation and hyperresponsiveness in a mouse model of allergic asthma. BALB/c mice sensitized and challenged with ovalbumin were administered paeonol intragastrically at a dose of 100 mg/kg daily. Paeonol significantly suppressed ovalbumin-induced airway hyperresponsiveness to acetylcholine chloride. Paeonol administration significantly inhibited the total inflammatory cell and eosinophil count in bronchoalveolar lavage fluid. Treatment with paeonol significantly enhanced IFN-γ levels and decreased interleukin-4 and interleukin-13 levels in bronchoalveolar lavage fluid and total immunoglobulin E levels in serum. Histological examination of lung tissue demonstrated that paeonol significantly attenuated allergen-induced lung eosinophilic inflammation and mucus-producing goblet cells in the airway. These data suggest that paeonol exhibits anti-inflammatory activity in allergic mice and may possess new therapeutic potential for the treatment of allergic bronchial asthma.

scholarly journals Immunomodulating Effects of HMR 3004 on Pulmonary Inflammation Caused by Heat-Killed Streptococcus pneumoniae in Mice

1998 ◽  
Vol 42 (12) ◽  
pp. 3309-3312 ◽  
Author(s):  
Michel Duong ◽  
Marie Simard ◽  
Yves Bergeron ◽  
Nathalie Ouellet ◽  
Mélanie Côté-Richer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Streptococcus Pneumoniae ◽  
Bronchoalveolar Lavage ◽  
Bacterial Pneumonia ◽  
Bronchoalveolar Lavage Fluid ◽  
Pulmonary Inflammation ◽  
Antimicrobial Properties ◽  
Fluorescein Isothiocyanate ◽  
Lavage Fluid ◽  
Lung Edema

ABSTRACT We investigated the influence of HMR 3004, a new ketolide antibiotic, on the pulmonary inflammation induced by heat-killed fluorescein isothiocyanate-labeled Streptococcus pneumoniae. HMR 3004 downregulated (P < 0.05) the pneumococcus-induced release of interleukin-6 (IL-6), IL-1β, and nitric oxide in bronchoalveolar lavage fluid. The drug limited (P < 0.05) neutrophil recruitment to lung tissues and alveoli but did not interfere with phagocytosis. HMR 3004 totally abrogated lung edema. By reducing inflammation in addition to possessing antimicrobial properties, HMR 3004 may participate in improving the outcome of bacterial pneumonia.

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