Estradiol in Severe Asthma with Premenstrual Worsening

Ensom, Mary H H; Chong, Gina; Beaudin, Bev; Bai, Tony R.

doi:10.1345/aph.1d090

Cited by 20 publications

(17 citation statements)

References 23 publications

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“…underlying this susceptibility remains unclear. Ensom and colleagues demonstrated the beneficial effects of estradiol in a severely asthmatic woman with premenstrual worsening of asthma (24).…”

Section: Discussionmentioning

confidence: 99%

Estrogen Determines Sex Differences in Airway Responsiveness after Allergen Exposure

Matsubara

Swasey

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et al. 2008

Am J Respir Cell Mol Biol

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The female hormone estrogen is an important factor in the regulation of airway function and inflammation, and sex differences in the prevalence of asthma are well described. Using an animal model, we determined how sex differences may underlie the development of altered airway function in response to allergen exposure. We compared sex differences in the development of airway hyperresponsiveness (AHR) after allergen exposure exclusively via the airways. Ovalbumin (OVA) was administered by nebulization on 10 consecutive days in BALB/c mice. After methacholine challenge, significant AHR developed in male mice but not in female mice. Ovariectomized female mice showed significant AHR after 10-day OVA inhalation. ICI182,780, an estrogen antagonist, similarly enhanced airway responsiveness even when administered 1 hour before assay. In contrast, 17b-estradiol dose-dependently suppressed AHR in male mice. In all cases, airway responsiveness was inhibited by the administration of a neurokinin 1 receptor antagonist. These results demonstrate that sex differences in 10-day OVAinduced AHR are due to endogenous estrogen, which negatively regulates airway responsiveness in female mice. Cumulatively, the results suggest that endogenous estrogen may regulate the neurokinin 1-dependent prejunctional activation of airway smooth muscle in allergen-exposed mice.Keywords: estrogen; sex; airway hyperresponsiveness; EFS; neuronal activation Sex differences have been described to play a role in various diseases, including atherosclerosis (1), osteoporosis (2), and certain neurologic disorders (3). Accumulating evidence suggests that hormonal factors are important in the expression of such sex differences at the phenotypic and genotypic levels. A number of epidemiologic and experimental reports suggest that the female hormone estrogen is an important factor in the regulation of airway function and inflammation. Estrogen can prevent cholinergic constriction of asthmatic tracheal rings in vitro (4), and estrogen treatment decreases airway responsiveness to acetylcholine in ovariectomized rats (5). On the other hand, female mice may be more susceptible than male mice to allergen-induced airway inflammation (6-8). The role of estrogen on sex differences in asthma has been the subject of much discussion (9, 10).There are many animal protocols for investigating allergeninduced airway hyperresponsiveness (AHR) and inflammation, with the majority using initial sensitization to allergen together with an adjuvant such as alum. Using this sensitization approach, some mouse studies have suggested a female superiority in the development of allergic airway inflammation (6-8). We examined the development of AHR after allergen exposure exclusively via the airways for 10 consecutive days in the absence of any adjuvant. Although AHR to inhaled methacholine (MCh) was not detected in female mice after 10-day ovalbumin (OVA) inhalation in vivo, electrical field stimulation (EFS) in vitro detected altered airway responsiveness. In large part, this EFS respon...

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Section: Discussionmentioning

confidence: 99%

Estrogen Determines Sex Differences in Airway Responsiveness after Allergen Exposure

Matsubara

Swasey

Loader

et al. 2008

Am J Respir Cell Mol Biol

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“…Several studies reported a reduction in asthma symptoms and corticosteroid requirement for asthma control in women with asthma who were given combined OC, estrogen, or gonadotropin releasing hormone analogue. 24,27,28,32,35 Because OC prevents luteinizing hormone surge and suppresses luteinizing hormone secretion, progesterone levels remain at a much lower level throughout the menstrual cycle in women taking OC compared with luteal phase levels of progesterone in women not taking OC. 11 Therefore, it is possible that the observed reduction in asthma symptoms with OC use may be a result of an absence of luteal phase increase in progesterone levels.…”

Section: Discussionmentioning

confidence: 99%

Endogenous and exogenous sex steroid hormones and asthma and wheeze in young women

Salam¹,

Wenten²,

Gilliland³

2006

Journal of Allergy and Clinical Immunology

124

102

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“…Changes occurring during sleep, in both non-rapid and rapid eye movement sleep stages, result in a shift from inhibitory to excitatory transmission to the AVPNs that could lead to worsening of airway function [Young et al 2005] (Figure 1). Similar mechanisms involving a decrease of tonic GABAergic inhibitory influences, may at least in part explain exercise- [McFadden and Gilbert, 1994] and premenstrual- [Ensom et al 2003] induced asthma. In the latter, it may involve a decrease of a GABA A receptor modulator, the 3-a-OH-dihydroprogesterone, which has an action similar to a neurosteroid.…”

Section: Central Mechanismsmentioning

confidence: 99%

Noninflammatory mechanisms of airway hyper-responsiveness in bronchial asthma: an overview

Baroffio

Barisione

Crimi

et al. 2009

Ther Adv Respir Dis

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Airway hyper-responsiveness (AHR) is a cardinal feature of asthma. Its absence has been considered useful in excluding asthma, whereas it may be present in other diseases such as atopic rhinitis and chronic obstructive pulmonary disease. AHR is often considered an epiphenomenon of airway inflammation. Actually, the response of airways to constrictor stimuli is modulated by a complex array of factors, some facilitating and others opposing airway narrowing. Thus, it has been suggested that AHR, and perhaps asthma, might be present even without or before the development of airway inflammation. We begin this review by highlighting some terminological and methodological issues concerning the measurement of AHR. Then we describe the neurohumoral mechanisms controlling airway tone. Finally, the pivotal role of airway smooth muscle and internal and external modulation of airway caliber in vivo are discussed in detail.

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Estradiol in Severe Asthma with Premenstrual Worsening

Cited by 20 publications

References 23 publications

Estrogen Determines Sex Differences in Airway Responsiveness after Allergen Exposure

Estrogen Determines Sex Differences in Airway Responsiveness after Allergen Exposure

Endogenous and exogenous sex steroid hormones and asthma and wheeze in young women

Noninflammatory mechanisms of airway hyper-responsiveness in bronchial asthma: an overview

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