scholarly journals Oleoylethanolamide induces eosinophilic airway inflammation in bronchial asthma

2021 ◽  
Author(s):  
Eun-Kyung Kwon ◽  
Youngwoo Choi ◽  
Il-Hee Yoon ◽  
Ha-Kyeong Won ◽  
Soyoon Sim ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Proinflammatory Cytokines ◽  
Airway Hyperresponsiveness ◽  
Bronchoalveolar Lavage Fluid ◽  
A549 Cells ◽  
Lavage Fluid ◽  
Lymphoid Cells ◽  
Eosinophil Activation

AbstractAsthma is a chronic eosinophilic inflammatory disease with an increasing prevalence worldwide. Endocannabinoids are known to have immunomodulatory biological effects. However, the contribution of oleoylethanolamide (OEA) to airway inflammation remains to be elucidated. To investigate the effect of OEA, the expression of proinflammatory cytokines was measured by RT-qPCR and ELISA in airway epithelial (A549) cells. The numbers of airway inflammatory cells and cytokine levels in bronchoalveolar lavage fluid, airway hyperresponsiveness, and type 2 innate lymphoid cells (ILC2s) were examined in BALB/c mice after 4 days of OEA treatment. Furthermore, eosinophil activation after OEA treatment was evaluated by measuring cellular CD69 levels in eosinophils from human peripheral eosinophils using flow cytometry. OEA induced type 2 inflammatory responses in vitro and in vivo. OEA increased the levels of proinflammatory cytokines, such as IL-6, IL-8, and IL-33, in A549 cells. In addition, it also induced eosinophilic inflammation, the production of IL-4, IL-5, IL-13, and IL-33 in bronchoalveolar lavage fluid, and airway hyperresponsiveness. OEA increased the numbers of IL-5- or IL-13-producing ILC2s in a mouse model. Finally, we confirmed that OEA increased CD69 expression (an eosinophil activation marker) on purified eosinophils from patients with asthma compared to those from healthy controls. OEA may play a role in the pathogenesis of asthma by activating ILC2s and eosinophils.

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.

Naringenin inhibits allergen-induced airway inflammation and airway responsiveness and inhibits NF-κB activity in a murine model of asthma

2009 ◽  
Vol 87 (9) ◽  
pp. 729-735 ◽  
Author(s):  
Ying Shi ◽  
Jian Dai ◽  
Hua Liu ◽  
Ruo-Ran Li ◽  
Pei-Li Sun ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Murine Model ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Binding Activity ◽  
Airway Reactivity ◽  
Total Ige ◽  
Serum Total Ige ◽  
Iκbα Degradation

Naringenin, a flavonoid, has antiinflammatory and immunomodulatory properties. We investigated whether naringenin could attenuate allergen-induced airway inflammation and its possible mechanism in a murine model of asthma. Mice were sensitized and challenged with ovalbumin. Some mice were administered with naringenin before ovalbumin challenge. We evaluated the development of airway inflammation and airway reactivity. Interleukin (IL)4, IL13, chemokine (C–C motif) ligand (CCL)5, and CCL11 in bronchoalveolar lavage fluid and serum total IgE were detected by ELISA. IκBα degradation and inducible nitric oxide synthase (iNOS) in lungs were measured by Western blot. We also tested NF-κB binding activity by electrophoretic mobility shift assay. The mRNA levels of iNOS, CCL5, and CCL11 were detected by real-time PCR. Naringenin attenuated ovalbumin-induced airway inflammation and airway reactivity in experimental mice. The naringenin-treated mice had lower levels of IL4 and IL13 in the bronchoalveolar lavage fluid and lower serum total IgE. Furthermore, naringenin inhibited pulmonary IκBα degradation and NF-κB DNA-binding activity. The levels of CCL5, CCL11, and iNOS were also significantly reduced. The results indicated that naringenin may play protective roles in the asthma process. The inhibition of NF-κB and the decreased expression of its target genes may account for this phenomenon.

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.

Relation of Interleukin-10 in Bronchoalveolar Lavage Fluid and Airway Inflammation in Bronchial Asthma

1999 ◽  
Vol 46 (1) ◽  
pp. 44
Author(s):  
Sook Young Lee ◽  
Hung Gue Youn ◽  
Youn Shin ◽  
Sang Haak Lee ◽  
Seok Chan Kim ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Bronchial Asthma ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Interleukin 10

scholarly journals The Omega-3 Fatty Acid Docosahexaenoic Acid Modulates Inflammatory Mediator Release in Human Alveolar Cells Exposed to Bronchoalveolar Lavage Fluid of ARDS Patients

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Paolo Cotogni ◽  
Antonella Trombetta ◽  
Giuliana Muzio ◽  
Marina Maggiora ◽  
Rosa Angela Canuto
Keyword(s):  
Docosahexaenoic Acid ◽  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Ex Vivo ◽  
A549 Cells ◽  
Lavage Fluid ◽  
Mediator Release ◽  
Omega 3 ◽  
Alveolar Cells ◽  
Cox 2

Background. This study investigated whether the 1 : 2 ω-3/ω-6 ratio may reduce proinflammatory response in human alveolar cells (A549) exposed to anex vivoinflammatory stimulus (bronchoalveolar lavage fluid (BALF) of acute respiratory distress syndrome (ARDS) patients).Methods. We exposed A549 cells to the BALF collected from 12 ARDS patients. After 18 hours, fatty acids (FA) were added as docosahexaenoic acid (DHA,ω-3) and arachidonic acid (AA,ω-6) in two ratios (1 : 2 or 1 : 7). 24 hours later, in culture supernatants were evaluated cytokines (TNF-α, IL-6, IL-8, and IL-10) and prostaglandins (PGE2and PGE3) release. The FA percentage content in A549 membrane phospholipids, content of COX-2, level of PPARγ, and NF-κB binding activity were determined.Results. The 1 : 2 DHA/AA ratio reversed the baseline predominance ofω-6 overω-3 in the cell membranes (P< 0.001). The proinflammatory cytokine release was reduced by the 1 : 2 ratio (P< 0.01 to <0.001) but was increased by the 1 : 7 ratio (P< 0.01). The 1 : 2 ratio reduced COX-2 and PGE2(P< 0.001) as well as NF-κB translocation into the nucleus (P< 0.01), while it increased activation of PPARγand IL-10 release (P< 0.001).Conclusion. This study demonstrated that shifting the FA supply fromω-6 toω-3 decreased proinflammatory mediator release in human alveolar cells exposed to BALF of ARDS patients.

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