The Role of Neural Inflammation in Asthma and Chronic Obstructive Pulmonary Disease

Joos, Guy; Swert, Katelijne O. De; Schelfhout, Vanessa; Pauwels, Romain

doi:10.1111/j.1749-6632.2003.tb03152.x

Cited by 53 publications

(25 citation statements)

References 87 publications

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“…The assumption is that these events trigger and up-regulate an NK-1-dependent pathway, leading to increases in ACh release. The role of NK receptors and their agonistic tachykinins in allergic airway inflammation is somewhat controversial (37). In a recent study, Boot and colleagues demonstrated that a NK1/ NK2 dual antagonist failed to modulate AHR and airway inflammation after allergen challenge in patients with asthma (38).…”

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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“…The release into the airways of tachykinins and neurokinins and the decrease of β 2 -adrenergic receptor, cholinesterase and neutral endopeptidase activities have been documented in these experimental conditions [3][4][5][6][7]60]. Conversely, reducing agents exert a relaxing effect on airway smooth muscle and they can inhibit bronchial smooth muscle contraction and prevent airway hyperresponsiveness in several experimental models [3][4][5][6][7]61].…”

Section: Asthmamentioning

confidence: 94%

Oxidants in Asthma and in Chronic Obstructive Pulmonary Disease (COPD)

Psarras¹,

Caramori²,

Contoli³

et al. 2005

CPD

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Experimental and clinical evidences suggest that oxidants play a role in the pathogenesis of respiratory disorders characterised by chronic airway inflammation such as asthma and chronic obstructive pulmonary disease (COPD). The respiratory system is chronically exposed to environmental pollutants, including oxidants. Exogenous sources of oxidants are particularly relevant to the pathogenesis of COPD, being cigarette smoke an extremely rich source of oxidants. In addition, the inflammatory cells recruited to the airways of patients with asthma and COPD, have an exceptional capacity to produce oxidants. Many decades of research have produced a significant amount of data indicating pro-oxidative molecular mechanisms putatively relevant in the pathogenesis of the oxidative stress which characterises these diseases, both locally and systemically. As a consequence, a drug therapy able to restore the redox imbalance in asthma and COPD would probably exert clinical and functional benefits. Indeed, currently available therapies for asthma and COPD can exert an inhibitory effect on oxidant production in the airways. However, it is unknown whether the efficacy of the treatment is somehow linked to the pharmacological modulation of the oxidant/antioxidant balance. So far, it appears that the potential role of antioxidant compounds in the treatment of asthma and COPD has not been fully explored.

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“…The mechanisms, including both allergic pathways (adaptive immunity) and nonallergic (innate) pathways, are implicated in asthma and contribute to the complexity of this disease (77). Therefore, the development of relevant models to study the mechanisms leading to the development of asthma is a great challenge (26,69). Current models mainly use allergic airway disease as an alternative for asthma, and many models are based on short-term, acute exposures to simple protein antigens, microorganisms, or chemical compounds (5).…”

Section: Chemokine Receptors In Chronic Lung Diseasesmentioning

confidence: 99%

Chemokine receptors and their therapeutic opportunities in diseased lung: Far beyond leukocyte trafficking

Tománková

Kriegová

Liu

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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Chemokine receptors and their chemokine ligands, key mediators of inflammatory and immune cell trafficking, are involved in the regulation of both physiological and pathological processes in the lung. The discovery that chemokine receptors/chemokines, typically expressed by inflammatory and immune cells, are also expressed in structural lung tissue cells suggests their role in mediating the restoration of lung tissue structure and functions. Thus, chemokine receptors/chemokines contribute not only to inflammatory and immune responses in the lung but also play a critical role in the regulation of lung tissue repair, regeneration, and remodeling. This review aims to summarize current state-of-the-art on chemokine receptors and their ligands in lung diseases such as chronic obstructive pulmonary disease, asthma/allergy, pulmonary fibrosis, acute lung injury, and lung infection. Furthermore, the therapeutic opportunities of chemokine receptors in aforementioned lung diseases are discussed. The review also aims to delineate the potential contribution of chemokine receptors to the processes leading to repair/regeneration of the lung tissue.

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The Role of Neural Inflammation in Asthma and Chronic Obstructive Pulmonary Disease

Cited by 53 publications

References 87 publications

Estrogen Determines Sex Differences in Airway Responsiveness after Allergen Exposure

Estrogen Determines Sex Differences in Airway Responsiveness after Allergen Exposure

Oxidants in Asthma and in Chronic Obstructive Pulmonary Disease (COPD)

Chemokine receptors and their therapeutic opportunities in diseased lung: Far beyond leukocyte trafficking

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