Quercetin 3-Glucoside-7-Rhamnoside from Hippophae rhamnosides L. Fruits Attenuate Allergy in Ovalbumin-Induced Allergic Mouse

Milk protein is one of the eight major allergens, and α–lactalbumin (α-LA) is one of the major allergens of bovine milk protein. Our previous studies found that Lactiplantibacillus plantarum HM-22...

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Allergic Inflammation Caused by Dimerized Translationally Controlled Tumor Protein is Attenuated by Cardamonin

Frontiers in Pharmacology ◽

10.3389/fphar.2021.765521 ◽

2021 ◽

Vol 12 ◽

Author(s):

Haejun Pyun ◽

Joo-Won Nam ◽

Hyunsoo Cho ◽

Jiyoung Park ◽

Eun Kyoung Seo ◽

...

Keyword(s):

Bronchoalveolar Lavage Fluid ◽

Allergic Inflammation ◽

Inflammatory Cells ◽

Allergic Diseases ◽

Lavage Fluid ◽

Specific Ige ◽

Translationally Controlled Tumor Protein ◽

Dimeric Form ◽

Allergic Mouse ◽

Inflammatory Effect

We demonstrated in our previous reports that dimeric form of translationally controlled tumor protein (dTCTP) initiates a variety of allergic phenomena. In the present study, we examined whether and how dTCTP’s role in allergic inflammation can be modulated or negated. The possible potential of cardamonin as an anti-allergic agent was assessed by ELISA using BEAS-2B cells and OVA-challenged allergic mouse model. The interaction between cardamonin and dTCTP was confirmed by SPR assay. Cardamonin was found to reduce the secretion of IL-8 caused by dTCTP in BEAS-2B cells by interacting with dTCTP. This interaction between dTCTP and cardamonin was confirmed through kinetic analysis (KD = 4.72 ± 0.07 μM). Also, cardamonin reduced the migration of various inflammatory cells in the bronchoalveolar lavage fluid (BALF), inhibited OVA specific IgE secretion and bronchial remodeling. In addition, cardamonin was observed to have an anti-allergic response by inhibiting the activity of NF-κB. Cardamonin exerts anti-allergic anti-inflammatory effect by inhibiting dTCTP, suggesting that it may be useful in the therapy of allergic diseases.

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Blocking ATP releasing channels prevents high extracellular ATP levels and airway hyperreactivity in an asthmatic mouse model

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00450.2020 ◽

2021 ◽

Author(s):

Llilian Arzola Martínez ◽

Rebeca Benavente ◽

Génesis Vega ◽

Mariana Ríos ◽

Wendy Fonseca ◽

...

Keyword(s):

Mouse Model ◽

Airway Inflammation ◽

Airway Epithelium ◽

Atp Release ◽

Specific Inhibitor ◽

Extracellular Atp ◽

Airway Hyperreactivity ◽

Luciferase Assay ◽

Asthmatic Patients ◽

Allergic Mouse

Allergic asthma is a chronic airway inflammatory response to different triggers like inhaled allergens. Excessive ATP in fluids from asthmatic patients is considered an inflammatory signal and an important autocrine/paracrine modulator of airway physiology. Here we investigated the deleterious effect of increased extracellular ATP (eATP) concentration on the mucociliary clearance (MCC) effectiveness and determined the role of ATP releasing channels during airway inflammation in an ovalbumin (OVA)-sensitized mouse model. Our allergic mouse model exhibited high levels of eATP measured in the tracheal fluid with a luciferin-luciferase assay and reduced MCC velocity determined by microspheres tracking in the trachea ex vivo. Addition of ATP had a dual effect on MCC, where lower ATP concentration (µM) increased microspheres velocity, while higher concentration (mM) transiently stopped microspheres movement. Also, an augmented ethidium bromide uptake by the allergic tracheal airway epithelium suggests an increase in ATP release channel functionality during inflammatory conditions. The use of carbenoxolone, a non-specific inhibitor of connexin and pannexin1channels reduced the eATP concentration in the allergic mouse tracheal fluid and dye uptake by the airway epithelium, providing evidence that these ATP release channels are facilitating the net flux of ATP to the lumen during airway inflammation. However, only the specific inhibition of pannexin1 with 10Panx peptide significantly reduced eATP in bronchoalveolar lavage and decreased airway hyperresponsiveness in OVA-allergic mouse model. These data provide evidence that blocking eATP may be a pharmacological alternative to be explored in rescue therapy during episodes of airflow restriction in asthmatic patients.

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Systemic And/Or Local Aerosol Inhibition Of S-Nitrosoglutathione Reductase (GSNOR) Ameliorates Physiologic, Biologic, And Proteomic Phenotypes In An Allergic Mouse Model Of Inflammatory Airway Disease

10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4075 ◽

2011 ◽

Author(s):

Loretta G. Que ◽

Matthew W. Foster ◽

Erin N. Potts ◽

Erik J. Soderblom ◽

Zhonghui Yang ◽

...

Keyword(s):

Mouse Model ◽

Airway Disease ◽

Inflammatory Airway Disease ◽

Allergic Mouse

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Acute and Chronic Exposure of Toluene Induces Genotoxicity in Different Regions of the Brain in Normal and Allergic Mouse Models

Neurotoxicity Research ◽

10.1007/s12640-019-00024-y ◽

2019 ◽

Vol 36 (4) ◽

pp. 669-678

Author(s):

Ting-Ying Laio ◽

Chih-Chun Chen ◽

Han-Hsing Tsou ◽

Tsung-Yun Liu ◽

Hsiang-Tsui Wang

Keyword(s):

Mouse Models ◽

Chronic Exposure ◽

Acute And Chronic Exposure ◽

The Brain ◽

Allergic Mouse

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Adenosine-mediated alteration of vascular reactivity and inflammation in a murine model of asthma

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01224.2007 ◽

2008 ◽

Vol 294 (5) ◽

pp. H2158-H2165 ◽

Cited By ~ 16

Author(s):

Dovenia S. Ponnoth ◽

Ahmed Nadeem ◽

S. Jamal Mustafa

Keyword(s):

Systemic Inflammation ◽

Endothelial Nitric Oxide Synthase ◽

Cardiovascular Events ◽

Vascular Reactivity ◽

Allergen Challenge ◽

Organ Bath ◽

Vascular Responses ◽

Oxide Synthase ◽

Endothelial Nitric Oxide ◽

Allergic Mouse

Chronic respiratory disorders such as asthma are believed to be associated with adverse cardiovascular events. We hypothesize that asthmatic inflammation translates into systemic inflammation and alters vascular responses where adenosine (AD) plays an important role. Therefore, this study investigated the effects of aerosolized AD, used to elevate lung AD levels, on vascular reactivity and inflammation in our allergic mouse model of asthma. Balb/c mice were divided into four groups: control (Con), Con + aerosolized AD (Con + AD), allergen sensitized and challenged (Sen), and Sen + aerosolized AD (Sen + AD). The animals were sensitized with ragweed (200 μg ip) on days 1 and 6, followed by 1% ragweed aerosol challenges from days 11 to 13. On day 14, the Con + AD and Sen + AD groups received a single AD aerosol challenge (6 mg/ml) for 2 min, followed by the collection of the aorta and plasma on day 15. Organ bath experiments showed concentration-dependent aortic relaxations to AD in the Con and Con + AD groups, which were impaired in the Sen and Sen + AD groups. Real-time PCR data showed changes in aortic AD receptors (ARs), with the expression of A1ARs upregulated, whereas the expression of A2ARs and endothelial nitric oxide synthase genes were downregulated, resulting in an impairment of vasorelaxation in the Sen and Sen + AD groups. The A1AR antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) reversed the impairment in vasorelaxation observed in the Sen and Sen + AD groups, whereas the A2BAR antagonist alloxazine inhibited vasorelaxation in all groups. Allergen challenge caused systemic inflammation in allergic mice, with AD aerosol further enhancing it as determined by the inflammatory cytokines profile in plasma. In conclusion, asthmatic mice showed altered vascular reactivity and systemic inflammation, with AD aerosol further exacerbating these effects.

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Characterization of adenosine receptor(s) involved in adenosine-induced bronchoconstriction in an allergic mouse model

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00353.2002 ◽

2003 ◽

Vol 284 (6) ◽

pp. L1012-L1019 ◽

Cited By ~ 33

Author(s):

Ming Fan ◽

Weixi Qin ◽

S. Jamal Mustafa

Keyword(s):

Mouse Model ◽

Adenosine Receptor ◽

Receptor Subtypes ◽

Dependent Manner ◽

Transcript Levels ◽

Allergen Sensitization ◽

Selective Agonist ◽

Dose Dependent ◽

Allergic Mouse

We recently reported that adenosine caused bronchoconstriction and enhanced airway inflammation in an allergic mouse model. In this study, we further report the characterization of the subtype of adenosine receptor(s) involved in bronchoconstriction. 5′-( N-ethylcarboxamido)adenosine (NECA), a nonselective adenosine agonist, elicited bronchoconstriction in a dose-dependent manner. Little effects of N 6-cyclopentyladenosine (A1-selective agonist) and 2- p-(2-carboxyethyl)phenethylamino-5′- N-ethylcarboxamidoadenosine (A2A-selective agonist) compared with NECA were observed in this model. 2-Chloro- N 6-(3-iodobenzyl)-9-[5-(methylcarbamoyl)-β-d-ribofuranosyl]adenosine, an A3-selective receptor agonist, produced a dose-dependent bronchoconstrictor response, which was blocked by selective A3 antagonist 2,3-diethyl-4,5-dipropyl-6-phenylpyridine-3-thiocarboxylate-5-carboxylate (MRS1523). However, MRS1523 only partially inhibited NECA-induced bronchoconstriction. Neither selective A1 nor A2A antagonists affected NECA-induced bronchoconstriction. Enprofylline, a relatively selective A2B receptor antagonist, blocked partly NECA-induced bronchoconstriction. Furthermore, a combination of enprofylline and MRS1523 completely abolished NECA-induced bronchoconstrictor response. Using RT-PCR, we found that all four adenosine receptor subtypes are expressed in control lungs. Allergen sensitization and challenge significantly increased transcript levels of the A2B and A3receptors, whereas the A1 receptor message decreased. No change in transcript levels of A2A receptors was observed after allergen sensitization and challenge. These findings suggest that A2B and A3 adenosine receptors play an important role in adenosine-induced bronchoconstriction in our allergic mouse model. Finally, whether the airway effects of the receptor agonists/antagonists are direct or indirect needs further investigations.

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