Advances in inhaled corticosteroid pharmacology

Zitt, Myron J.

doi:10.2500/aap.2007.28.2989

Cited by 9 publications

(5 citation statements)

References 39 publications

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“…Corticosteroid treatment clearly suppresses inflammation in a large majority of asthmatic patients [136–139] and in mouse asthma models of allergen-induced airway inflammation [137, 140], though it is clear that corticosteroids do not alter the natural history of asthma [139]. In addition to the effects on the number and function of inflammatory cells that ordinarily infiltrate the airway mucosa in chronic asthma, CS treatment also inhibits the release of inflammatory mediators secreted by epithelial cells such as RANTES [141], GM-CSF [142], and eotaxin [143].…”

Section: Apoptosis In Airway Epithelium In Diseasementioning

confidence: 99%

Apoptosis and the Airway Epithelium

White

2011

Journal of Allergy

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The airway epithelium functions as a barrier and front line of host defense in the lung. Apoptosis or programmed cell death can be elicited in the epithelium as a response to viral infection, exposure to allergen or to environmental toxins, or to drugs. While apoptosis can be induced via activation of death receptors on the cell surface or by disruption of mitochondrial polarity, epithelial cells compared to inflammatory cells are more resistant to apoptotic stimuli. This paper focuses on the response of airway epithelium to apoptosis in the normal state, apoptosis as a potential regulator of the number and types of epithelial cells in the airway, and the contribution of epithelial cell apoptosis in important airways diseases.

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Section: Apoptosis In Airway Epithelium In Diseasementioning

confidence: 99%

Apoptosis and the Airway Epithelium

White

2011

Journal of Allergy

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“…Indeed, although the anti-inflammatory and bronchodilatory capabilities of inhaled corticosteroids and long-acting ␤ 2 -agonists, respectively, have been well documented, the consequences of these interventions on airway structure and function remain either controversial or poorly understood (reviewed in Ref. 41).…”

mentioning

confidence: 99%

Combined budesonide/formoterol therapy in conjunction with allergen avoidance ameliorates house dust mite-induced airway remodeling and dysfunction

Johnson

Pacitto²,

Wong³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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5, 2008; doi:10.1152/ajplung.90229.2008.-Allergic asthma is characterized by airway inflammation in response to chronic allergen exposure, resulting in remodeling of the airway wall accompanied by dysfunctional airway physiology. However, a link between the immune-inflammatory response to allergen and changes to airway structure and physiology has not yet been fully elucidated. Moreover, the impact of inhaled corticosteroids and ␤2-agonists, the primary pharmacotherapy for asthma, on this process has not been completely evaluated. In this study, we employed a murine model of chronic exposure to a common environmental aeroallergen, house dust mite, to recapitulate the phenotype of clinical asthma. By examining the therapeutic effects of corticosteroid/␤ 2-agonist combination therapy with budesonide/formoterol (BUD/FORM) in this model of airway disease, we endeavored to determine the impact of BUD/FORM on lung inflammation, structure, and physiology. BUD/FORM was delivered either while allergen exposure was ongoing (concurrent therapy) or following the cessation of allergen exposure (postexposure therapy). Our results show that airway inflammation was substantially reduced in BUD/FORM-treated mice in the concurrent therapy group, whereas in the postexposure therapy group airway inflammation spontaneously resolved. In contrast, BUD/FORM was most effective in resolving several aspects of airway remodeling and bronchial hyperreactivity when delivered in conjunction with allergen withdrawal. This study demonstrates that although both BUD/FORM therapy and allergen avoidance independently reduce airway inflammation, only BUD/FORM therapy in conjunction with allergen avoidance can effectively reverse airway remodeling and bronchial hyperreactivity induced by chronic allergen exposure.

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“…But, interestingly, although it has been manifested that antihistamines decrease the asthma symptoms and increase the quality of life; generally, they do not recover the objective measures of lung functions in dosages sufficient to control the allergic rhinitis. This effect can be obtained potentially by higher doses [10]. The usage of H1 antihistamines in children with asthma is not harmful and it in fact, proves to be beneficial in children with mild asthma.…”

Section: The Antiallergic Effectsmentioning

confidence: 97%

Action Mechanism of Antihistamines and the New Antihistamines

Neslihan¹,

Uslu

2005

CMCAIAA

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Antihistamines have an important role in dermatology. In order to understand how antihistamines work, effects of histamine should be examined first. Histamine was first defined in 1920s and was shown to take part in the pathogenesis of diseases such as urticaria, anaphylaxis, asthma, and allergic rhinitis. The main goal in the treatment of urticaria and other diseases related to histamine is to keep this powerful mediator's effects under control. So many antihistamines have been presented to the market since 1942 and still, new compounds are being developed. For years, antihistamines have been categorized as first, second and third generation. In this text, a review of the action mechanism of antihistamines and the new antihistamines will be presented.

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Advances in inhaled corticosteroid pharmacology

Cited by 9 publications

References 39 publications

Apoptosis and the Airway Epithelium

Apoptosis and the Airway Epithelium

Combined budesonide/formoterol therapy in conjunction with allergen avoidance ameliorates house dust mite-induced airway remodeling and dysfunction

Action Mechanism of Antihistamines and the New Antihistamines

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