Journal articles: 'Airway (Medicine) - Inflammation'

1

Shelhamer, James H. "Airway Inflammation." Annals of Internal Medicine 123, no. 4 (August 15, 1995): 288. http://dx.doi.org/10.7326/0003-4819-123-4-199508150-00008.

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O’Byrne, Paul M. "Airway Inflammation and Airway Hyperresponsiveness." Chest 90, no. 4 (October 1986): 575–77. http://dx.doi.org/10.1378/chest.90.4.575.

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Finsnes, Finn, Torstein Lyberg, Geir Christensen, and Ole H. Skjønsberg. "Effect of endothelin antagonism on the production of cytokines in eosinophilic airway inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 4 (April 1, 2001): L659—L665. http://dx.doi.org/10.1152/ajplung.2001.280.4.l659.

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Endothelin (ET)-1 has been launched as an important mediator in bronchial asthma, which is an eosinophilic airway inflammation. However, the interplay between ET-1 and other proinflammatory mediators during the development of airway inflammation has not been elucidated. We wanted to study 1) whether the production of ET-1 precedes the production of other proinflammatory mediators and 2) whether ET-1 stimulates the production of these mediators within the airways. These hypotheses were studied during the development of an eosinophilic airway inflammation in rats. The increase in ET-1 mRNA level in lung tissue preceded the increase in mRNA levels of tumor necrosis factor-α, interleukin (IL)-1β, and IL-8. Treatment of the animals with the ET receptor antagonist bosentan resulted in a substantial decrease in the concentrations of tumor necrosis factor-α, IL-4, IL-1β, interferon-γ, and ET-1 in bronchoalveolar lavage fluid. In conclusion, the synthesis of ET-1 as measured by increased mRNA level precedes the synthesis of other proinflammatory cytokines of importance for the development of an eosinophilic airway inflammation, and ET antagonism inhibits the production of these mediators within the airways. Whether treatment with ET antagonists will prove beneficial for patients with eosinophilic airway inflammations like bronchial asthma is not yet known.

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Taylor, D. R., and D. C. Cowan. "Assessing airway inflammation." Thorax 65, no. 12 (October 11, 2010): 1031–32. http://dx.doi.org/10.1136/thx.2009.132985.

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Kalla, Ismail S. "Measuring Airway Inflammation." Clinical Pulmonary Medicine 22, no. 2 (March 2015): 53–61. http://dx.doi.org/10.1097/cpm.0000000000000081.

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Marianne, Frieri. "Human Airway Inflammation." Annals of Allergy, Asthma & Immunology 88, no. 3 (March 2002): 343. http://dx.doi.org/10.1016/s1081-1206(10)62020-0.

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7

Balter, Meyer S. "Treating airway inflammation." Asthma Magazine 1, no. 5 (September 1996): 24–26. http://dx.doi.org/10.1016/s1088-0712(96)80011-2.

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Agrawal, Devendra K., and Arpita Bharadwaj. "Allergic airway inflammation." Current Allergy and Asthma Reports 5, no. 2 (March 2005): 142–48. http://dx.doi.org/10.1007/s11882-005-0088-7.

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9

Leff, A. R., K. J. Hamann, and C. D. Wegner. "Inflammation and cell-cell interactions in airway hyperresponsiveness." American Journal of Physiology-Lung Cellular and Molecular Physiology 260, no. 4 (April 1, 1991): L189—L206. http://dx.doi.org/10.1152/ajplung.1991.260.4.l189.

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Airway hyperresponsiveness results from the conversion of normally reactive airways to a state of augmented responsiveness to constrictor stimuli. Although the mechanism accounting for the induction of airway hyperresponsiveness remains elusive, recent investigations have suggested that inflammation may be a sine qua non for human asthma. Numerous experimental models have demonstrated the necessity of circulating granulocytes as mediators of augmented bronchoconstriction during immune challenge. It is not known how granulocytes are targeted for selective migration to the conducting airways of the lung during hyperresponsive states; however, recent evidence implicates the upregulation of granulocyte adhesion molecules on both the endothelial and epithelial surfaces of the airway. There is evidence that during migration diapedesis, granulocytes interact with epithelial and endothelial cells to produce regionally secreted mediators that upregulate the responsiveness of adjacent airway smooth muscle and/or cause lumenal edema, thus augmenting the effect of constrictor stimuli. Most evidence suggests that the eosinophil is the most important granulocyte in these responses and that eosinophilic infiltration and activation may account for the unique, spasmodic, and cyclic nature of hyperreactive airways. The molecular biology of the eosinophil granule proteins has characterized four distinct substances, each of which exerts potential cytotoxic effects on airway epithelium by different mechanism. In addition, at least one of these proteins, the major basic protein, appears to cause direct, noncytotoxic stimulation of epithelial secretion that upregulates nonspecifically the response of airway smooth muscle to contractile stimuli. The recognition of inflammation as the essential component to airway hyperresponsiveness provides a fresh approach to a difficult problem and suggests a host of novel therapies for human asthma.

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Dolovich, J., and F. E. Hargreave. "Airway Mucosal Inflammation." Journal of Asthma 29, no. 3 (January 1992): 145–49. http://dx.doi.org/10.3109/02770909209099022.

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Brightling, Christopher, and Neil Greening. "Airway inflammation in COPD: progress to precision medicine." European Respiratory Journal 54, no. 2 (May 9, 2019): 1900651. http://dx.doi.org/10.1183/13993003.00651-2019.

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Chronic obstructive pulmonary disease (COPD) is a significant cause of morbidity and mortality worldwide, and its prevalence is increasing. Airway inflammation is a consistent feature of COPD and is implicated in the pathogenesis and progression of COPD, but anti-inflammatory therapy is not first-line treatment. The inflammation has many guises and phenotyping this heterogeneity has revealed different patterns. Neutrophil-associated COPD with activation of the inflammasome, T1 and T17 immunity is the most common phenotype with eosinophil-associated T2-mediated immunity in a minority and autoimmunity observed in more severe disease. Biomarkers have enabled targeted anti-inflammatory strategies and revealed that corticosteroids are most effective in those with evidence of eosinophilic inflammation, whereas, in contrast to severe asthma, response to anti-interleukin-5 biologicals in COPD has been disappointing, with smaller benefits for the same intensity of eosinophilic inflammation questioning its role in COPD. Biological therapies beyond T2-mediated inflammation have not demonstrated benefit and in some cases increased risk of infection, suggesting that neutrophilic inflammation and inflammasome activation might be largely driven by bacterial colonisation and dysbiosis. Herein we describe current and future biomarker approaches to assess inflammation in COPD and how this might reveal tractable approaches to precision medicine and unmask important host–environment interactions leading to airway inflammation.

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Hunt, E. B., A. Sullivan, J. Galvin, J. MacSharry, and D. M. Murphy. "Gastric Aspiration and Its Role in Airway Inflammation." Open Respiratory Medicine Journal 12, no. 1 (January 23, 2018): 1–10. http://dx.doi.org/10.2174/1874306401812010001.

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Gastro-Oesophageal Reflux (GOR) has been associated with chronic airway diseases while the passage of foreign matter into airways and lungs through aspiration has the potential to initiate a wide spectrum of pulmonary disorders. The clinical syndrome resulting from such aspiration will depend both on the quantity and nature of the aspirate as well as the individual host response. Aspiration of gastric fluids may cause damage to airway epithelium, not only because acidity is toxic to bronchial epithelial cells but also due to the effect of digestive enzymes such as pepsin and bile salts. Experimental models have shown that direct instillation of these factors to airways epithelia cause damage with a consequential inflammatory response. The pathophysiology of these responses is gradually being dissected, with better understanding of acute gastric aspiration injury, a major cause of acute lung injury, providing opportunities for therapeutic intervention and potentially, ultimately, improved understanding of the chronic airway response to aspiration. Ultimately, clarification of the inflammatory pathways which are related to micro-aspirationviapepsin and bile acid salts may eventually progress to pharmacological intervention and surgical studies to assess the clinical benefits of such therapies in driving symptom improvement or reducing disease progression.

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13

Barnes, N. C., and J. F. Costello. "Airway hyperresponsiveness and inflammation." British Medical Bulletin 43, no. 2 (April 1987): 445–59. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072193.

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Banno, Asoka, Aravind T. Reddy, Sowmya P. Lakshmi, and Raju C. Reddy. "Bidirectional interaction of airway epithelial remodeling and inflammation in asthma." Clinical Science 134, no. 9 (May 2020): 1063–79. http://dx.doi.org/10.1042/cs20191309.

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Abstract Asthma is a chronic disease of the airways that has long been viewed predominately as an inflammatory condition. Accordingly, current therapeutic interventions focus primarily on resolving inflammation. However, the mainstay of asthma therapy neither fully improves lung function nor prevents disease exacerbations, suggesting involvement of other factors. An emerging concept now holds that airway remodeling, another major pathological feature of asthma, is as important as inflammation in asthma pathogenesis. Structural changes associated with asthma include disrupted epithelial integrity, subepithelial fibrosis, goblet cell hyperplasia/metaplasia, smooth muscle hypertrophy/hyperplasia, and enhanced vascularity. These alterations are hypothesized to contribute to airway hyperresponsiveness, airway obstruction, airflow limitation, and progressive decline of lung function in asthmatic individuals. Consequently, targeting inflammation alone does not suffice to provide optimal clinical benefits. Here we review asthmatic airway remodeling, focusing on airway epithelium, which is critical to maintaining a healthy respiratory system, and is the primary defense against inhaled irritants. In asthma, airway epithelium is both a mediator and target of inflammation, manifesting remodeling and resulting obstruction among its downstream effects. We also highlight the potential benefits of therapeutically targeting airway structural alterations. Since pathological tissue remodeling is likewise observed in other injury- and inflammation-prone tissues and organs, our discussion may have implications beyond asthma and lung disease.

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15

Gross, Nicholas J. "Airway Inflammation in COPD." Chest 107, no. 5 (May 1995): 210S—213S. http://dx.doi.org/10.1378/chest.107.5_supplement.210s.

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16

Lemanske, R. F. "Mechanisms of airway inflammation." Chest 101, no. 6 (June 1, 1992): 372S—377. http://dx.doi.org/10.1378/chest.101.6.372s.

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Lemanske, Robert F. "Mechanisms of Airway Inflammation." Chest 101, no. 6 (June 1992): 372S—377S. http://dx.doi.org/10.1378/chest.101.6_supplement.372s.

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18

O'Byrne, Paul M., Frederick E. Hargreave, and John G. Kirby. "Airway Inflammation and Hyperresponsiveness." American Review of Respiratory Disease 136, no. 4_pt_2 (October 1987): S35—S37. http://dx.doi.org/10.1164/ajrccm/136.4_pt_2.s35.

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19

KleinJan, Alex. "Airway inflammation in asthma." Current Opinion in Pulmonary Medicine 22, no. 1 (January 2016): 46–52. http://dx.doi.org/10.1097/mcp.0000000000000224.

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Eastwood, Peter R. "Respirology supplement: Airway inflammation." Respirology 18 (November 2013): 1. http://dx.doi.org/10.1111/resp.12195.

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Brusasco, Vito, Emanuele Crimi, and Riccardo Pellegrino. "Airway Inflammation in COPD." American Journal of Respiratory and Critical Care Medicine 176, no. 5 (September 2007): 425–26. http://dx.doi.org/10.1164/rccm.200706-820ed.

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22

Russell, Richard J., and Christopher Brightling. "Pathogenesis of asthma: implications for precision medicine." Clinical Science 131, no. 14 (June 30, 2017): 1723–35. http://dx.doi.org/10.1042/cs20160253.

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The pathogenesis of asthma is complex and multi-faceted. Asthma patients have a diverse range of underlying dominant disease processes and pathways despite apparent similarities in clinical expression. Here, we present the current understanding of asthma pathogenesis. We discuss airway inflammation (both T2HIGH and T2LOW), airway hyperresponsiveness (AHR) and airways remodelling as four key factors in asthma pathogenesis, and also outline other contributory factors such as genetics and co-morbidities. Response to current asthma therapies also varies greatly, which is probably related to the inter-patient differences in pathogenesis. Here, we also summarize how our developing understanding of detailed pathological processes potentially translates into the targeted treatment options we require for optimal asthma management in the future.

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23

Dakhama, Azzeddine, Jung-Won Park, Christian Taube, Mohamed El Gazzar, Taku Kodama, Nobuaki Miyahara, Katsuyuki Takeda, et al. "Alteration of airway neuropeptide expression and development of airway hyperresponsiveness following respiratory syncytial virus infection." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 4 (April 2005): L761—L770. http://dx.doi.org/10.1152/ajplung.00143.2004.

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The mechanisms by which respiratory syncytial virus (RSV) infection causes airway hyperresponsiveness (AHR) are not fully established. We hypothesized that RSV infection may alter the expression of airway sensory neuropeptides, thereby contributing to the development of altered airway function. BALB/c mice were infected with RSV followed by assessment of airway function, inflammation, and sensory neuropeptide expression. After RSV infection, mice developed significant airway inflammation associated with increased airway resistance to inhaled methacholine and increased tracheal smooth muscle responsiveness to electrical field stimulation. In these animals, substance P expression was markedly increased, whereas calcitonin gene-related peptide (CGRP) expression was decreased in airway tissue. Prophylactic treatment with Sendide, a highly selective antagonist of the neurokinin-1 receptor, or CGRP, but not the CGRP antagonist CGRP(8–37), inhibited the development of airway inflammation and AHR in RSV-infected animals. Therapeutic treatment with CGRP, but not CGRP(8–37) or Sendide, abolished AHR in RSV-infected animals despite increased substance P levels and previously established airway inflammation. These data suggest that RSV-induced airway dysfunction is, at least in part, due to an imbalance in sensory neuropeptide expression in the airways. Restoration of this balance may be beneficial for the treatment of RSV-mediated airway dysfunction.

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Chiba, Yoshihiko, Takashi Kusakabe, and Shioko Kimura. "Decreased expression of uteroglobin-related protein 1 in inflamed mouse airways is mediated by IL-9." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 6 (December 2004): L1193—L1198. http://dx.doi.org/10.1152/ajplung.00263.2004.

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Uteroglobin-related protein 1 (UGRP1) is a secretory protein, highly expressed in epithelial cells of airways. Although an involvement of UGRP1 in the pathogenesis of asthma has been suggested, its function in airways remains unclear. In the present study, a relationship between airway inflammation, UGRP1 expression, and interleukin-9 (IL-9), an asthma candidate gene, was evaluated by using a murine model of allergic bronchial asthma. A severe airway inflammation accompanied by airway eosinophilia and elevation of IL-9 in bronchoalveolar lavage (BAL) fluids was observed after ovalbumin (OVA) challenge to OVA-sensitized mice. In this animal model of airway inflammation, lung Ugrp1 mRNA expression was greatly decreased compared with control mice. A significant inverse correlation between lung Ugrp1 mRNA levels and IL-9 levels in BAL fluid was demonstrated by regression analysis ( r = 0.616, P = 0.023). Immunohistochemical analysis revealed a distinct localization of UGRP1 in airway epithelial cells of control mice, whereas UGRP1 staining was patchy and faint in inflamed airways. Intranasal administration of IL-9 to naive mice decreased the level of Ugrp1 expression in lungs. These findings suggest that UGRP1 is downregulated in inflamed airways, such as allergic asthmatics, and IL-9 might be an important mediator for modulating UGRP1 expression.

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Lee, Bao-Hong, Yu-Hsiang Cheng, and She-Ching Wu. "Graptopetalum paraguayenseAmeliorates Airway Inflammation and Allergy in Ovalbumin- (OVA-) Sensitized BALB/C Mice by Inhibiting Th2 Signal." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/237096.

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Role of inflammation-induced oxidative stress in the pathogenesis and progression of chronic inflammatory airways diseases has received increasing attention in recent years. Nuclear factor erythroid 2-related factor 2 is the primary transcription factor that regulates the expression of antioxidant and detoxifying enzymes.Graptopetalum paraguayenseE. Walther, a vegetable consumed in Taiwan, has been used in folk medicine for protection against liver injury through elevating antioxidation. Recently, we found that gallic acid is an active compound ofGraptopetalum paraguayenseE. Walther, which has been reported to inhibit T-helper 2 cytokines. Currently, we assumed thatGraptopetalum paraguayenseE. Walther may potentially protect against ovalbumin-induced allergy and airway inflammation. Results demonstrated thatGraptopetalum paraguayenseE. Walther ethanolic extracts (GPE) clearly inhibited airway inflammation, mucus cell hyperplasia, and eosinophilia in OVA-challenged mice. Additionally, GPE also prevented T-cell infiltration and Th2 cytokines, including interleukin- (IL-)4, IL-5, and IL-13 generations in bronchial alveolar lavage fluid. The adhesion molecules ICAM-1 and VCAM-1 were substantially reduced by GPE treatment mediated by Nrf2 activation. Moreover, GPE attenuated GATA3 expression and inhibited Th2 signals of the T cells. These findings suggested that GPE ameliorated the development of airway inflammation through immune regulation.

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Pohunek, Petr. "Inflammation and airway remodeling." Pediatric Pulmonology 37, S26 (2004): 98–99. http://dx.doi.org/10.1002/ppul.70067.

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Đurđević, Nataša, Branislava Milenković, Jelena Janković, Javorka Mitić, Slobodan Belić, Elena Jordanova, and Marko Baralić. "Airway inflammation in patients with bronchiectasis." Halo 194 27, no. 2 (2021): 68–72. http://dx.doi.org/10.5937/halo27-31410.

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Bronchiectasis is a chronic lung disease characterized by an abnormal dilation of the bronchial lumen caused by weakening or destruction of the muscle or elastic components of the bronchial wall, decreased mucous clearance and frequent infections of the respiratory tract. The golden standard for bronchiectasis diagnosis is high-resolution computed tomography (HRCT) of the chest. Inflammation holds a central role in the development of structural lung changes, as well as airway and lung parenchyma damage. Infection and colonization of the respiratory tract contribute to increased inflammation and further damage to the lung. Upon entry into the respiratory tract, the pathogens activate epithelial cells, macrophages and dendritic cells. Activated inflammatory cells secrete chemical mediators which activate the immune response and thus allow the phagocytosis of pathogens. Early diagnosis, appropriate treatment and interruption of the vicious circle between infection and inflammation in patients suffering from bronchiectasis, prevent the development of structural changes to the airways.

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Uryasjev, M. O., I. V. Ponomareva, M. F. Bhar, and S. I. Glotov. "The cough variant asthma." Terapevticheskii arkhiv 92, no. 3 (April 27, 2020): 98–101. http://dx.doi.org/10.26442/00403660.2020.03.000404.

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Cough variant asthma (CVA) was first described by W. Corrao. CVA was described as the isolated chronic cough as the only presenting symptom responsive to bronchodilator therapy.This phenotype of asthma is present with airway hyperresponsiveness, eosinophilic inflammation airways and bronchodilator responsive coughing without typical manifestation of asthma such as wheezing or dyspnea. CVA shares common features with classic asthma such as eosinophilic inflammation and airway remodeling. Because of that, CVA is clinically considered as a variant type of asthma.

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Regnard, J., M. Beji, and I. Jallat-Daloz. "Airway Inflammation Affects Airway and Distal Circulatory Control." Archives of Physiology and Biochemistry 111, no. 4 (January 2003): 347–51. http://dx.doi.org/10.3109/13813450312331337577.

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J., Regnard, Beji M., and Jallat-Daloz I. "Airway Inflammation Affects Airway and Distal Circulatory Control." Archives of Physiology and Biochemistry 111, no. 4 (April 1, 2003): 347–51. http://dx.doi.org/10.1080/13813450312331337577.

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Jha, Aruni, Pawan Sharma, Vidyanand Anaparti, Min H. Ryu, and Andrew J. Halayko. "A role for transient receptor potential ankyrin 1 cation channel (TRPA1) in airway hyper-responsiveness?" Canadian Journal of Physiology and Pharmacology 93, no. 3 (March 2015): 171–76. http://dx.doi.org/10.1139/cjpp-2014-0417.

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Airway smooth muscle (ASM) contraction controls the airway caliber. Airway narrowing is exaggerated in obstructive lung diseases, such as asthma and chronic obstructive pulmonary disease (COPD). The mechanism by which ASM tone is dysregulated in disease is not clearly understood. Recent research on ion channels, particularly transient receptor potential cation channel, subfamily A, member 1 (TRPA1), is uncovering new understanding of altered airway function. TRPA1, a member of the TRP channel superfamily, is a chemo-sensitive cation channel that can be activated by a variety of external and internal stimuli, leading to the influx of Ca2+. Functional TRPA1 channels have been identified in neuronal and non-neuronal tissues of the lung, including ASM. In the airways, these channels can regulate the release of mediators that are markers of airway inflammation in asthma and COPD. For, example, TRPA1 controls cigarette-smoke-induced inflammatory mediator release and Ca2+ mobilization in vitro and in vivo, a response tied to disease pathology in COPD. Recent work has revealed that pharmacological or genetic inhibition of TRPA1 inhibits the allergen-induced airway inflammation in vitro and airway hyper-responsiveness (AHR) in vivo. Collectively, it appears that TRPA1 channels may be determinants of ASM contractility and local inflammation control, positioning them as part of novel mechanisms that control (patho)physiological function of airways and ASM.

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Steelant, B., S. F. Seys, G. Boeckxstaens, C. A. Akdis, J. L. Ceuppens, and P. W. Hellings. "Restoring airway epithelial barrier dysfunction: a new therapeutic challenge in allergic airway disease." Rhinology journal 54, no. 3 (September 1, 2016): 195–205. http://dx.doi.org/10.4193/rhino15.376.

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An intact functional mucosal barrier is considered to be crucial for the maintenance of airway homeostasis as it protects the host immune system from exposure to allergens and noxious environmental triggers. Recent data provided evidence for the contribution of barrier dysfunction to the development of inflammatory diseases in the airways, skin and gut. A defective barrier has been documented in chronic rhinosinusitis, allergic rhinitis, asthma, atopic dermatitis and inflammatory bowel diseases. However, it remains to be elucidated to what extent primary (genetic) versus secondary (inflammatory) mechanisms drive barrier dysfunction. The precise pathogenesis of barrier dysfunction in patients with chronic mucosal inflammation and its implications on tissue inflammation and systemic absorption of exogenous particles are only partly understood. Since epithelial barrier defects are linked with chronicity and severity of airway inflammation, restoring the barrier integrity may become a useful approach in the treatment of allergic diseases. We here provide a state-of-the-art review on epithelial barrier dysfunction in upper and lower airways as well as in the intestine and the skin and on how barrier dysfunction can be restored from a therapeutic perspective.

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Ford, William R., Alan E. Blair, Rhys L. Evans, Elinor John, Joachim J. Bugert, Kenneth J. Broadley, and Emma J. Kidd. "Human parainfluenza type 3 virus impairs the efficacy of glucocorticoids to limit allergy-induced pulmonary inflammation in guinea-pigs." Clinical Science 125, no. 10 (July 16, 2013): 471–82. http://dx.doi.org/10.1042/cs20130130.

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Viral exacerbations of allergen-induced pulmonary inflammation in pre-clinical models reportedly reduce the efficacy of glucocorticoids to limit pulmonary inflammation and airways hyper-responsiveness to inhaled spasmogens. However, exacerbations of airway obstruction induced by allergen challenge have not yet been studied. hPIV-3 (human parainfluenza type 3 virus) inoculation of guinea-pigs increased inflammatory cell counts in BAL (bronchoalveolar lavage) fluid and caused hyper-responsiveness to inhaled histamine. Both responses were abolished by treatment with either dexamethasone (20 mg/kg of body weight, subcutaneous, once a day) or fluticasone propionate (a 0.5 mg/ml solution aerosolized and inhaled over 15 min, twice a day). In ovalbumin-sensitized guinea-pigs, allergen (ovalbumin) challenge caused two phases of airway obstruction [measured as changes in sGaw (specific airways conductance) using whole body plethysmography]: an immediate phase lasting between 4 and 6 h and a late phase at about 7 h. The late phase, airway hyper-responsiveness to histamine and inflammatory cell counts in BAL were all significantly reduced by either glucocorticoid. Inoculation of guinea-pigs sensitized to ovalbumin with hPIV-3 transformed the allergen-induced airway obstruction from two transient phases into a single sustained response lasting up to 12 h. This exacerbated airway obstruction and airway hyper-responsiveness to histamine were unaffected by treatment with either glucocorticoid whereas inflammatory cell counts in BAL were only partially inhibited. Virus- or allergen-induced pulmonary inflammation, individually, are glucocorticoid-sensitive, but in combination generate a phenotype where glucocorticoid efficacy is impaired. This suggests that during respiratory virus infection, glucocorticoids might be less effective in limiting pulmonary inflammation associated with asthma.

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Boushey, Homer A. "Airway Inflammation and Severe Asthma." JAMA 279, no. 11 (March 18, 1998): 883. http://dx.doi.org/10.1001/jama.279.11.883.

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Siddiqui, Salman, and Christopher E. Brightling. "Airways Disease: Phenotyping Heterogeneity Using Measures of Airway Inflammation." Allergy, Asthma, and Clinical Immunology 03, no. 02 (2007): 60. http://dx.doi.org/10.2310/7480.2007.00005.

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Siddiqui, Salman, and Christopher E. Brightling. "Airways Disease: Phenotyping Heterogeneity Using Measures of Airway Inflammation." Allergy, Asthma & Clinical Immunology 3, no. 2 (2007): 60. http://dx.doi.org/10.1186/1710-1492-3-2-60.

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37

Fine, Jonathan M., and John R. Balmes. "Airway Inflammation and Occupational Asthma." Clinics in Chest Medicine 9, no. 4 (December 1988): 577–90. http://dx.doi.org/10.1016/s0272-5231(21)00583-9.

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Morianos, Ioannis, and Maria Semitekolou. "Dendritic Cells: Critical Regulators of Allergic Asthma." International Journal of Molecular Sciences 21, no. 21 (October 26, 2020): 7930. http://dx.doi.org/10.3390/ijms21217930.

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Allergic asthma is a chronic inflammatory disease of the airways characterized by airway hyperresponsiveness (AHR), chronic airway inflammation, and excessive T helper (Th) type 2 immune responses against harmless airborne allergens. Dendritic cells (DCs) represent the most potent antigen-presenting cells of the immune system that act as a bridge between innate and adaptive immunity. Pertinent to allergic asthma, distinct DC subsets are known to play a central role in initiating and maintaining allergen driven Th2 immune responses in the airways. Nevertheless, seminal studies have demonstrated that DCs can also restrain excessive asthmatic responses and thus contribute to the resolution of allergic airway inflammation and the maintenance of pulmonary tolerance. Notably, the transfer of tolerogenic DCs in vivo suppresses Th2 allergic responses and protects or even reverses established allergic airway inflammation. Thus, the identification of novel DC subsets that possess immunoregulatory properties and can efficiently control aberrant asthmatic responses is critical for the re-establishment of tolerance and the amelioration of the asthmatic disease phenotype.

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Aleva, Roelof M., Jan Kraan, Mieke Smith, Nick H. T. Ten Hacken, Dirkje S. Postma, and Wim Timens. "Techniques in Human Airway Inflammation." Chest 113, no. 1 (January 1998): 182–85. http://dx.doi.org/10.1378/chest.113.1.182.

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Hanania, Nicola A. "Targeting Airway Inflammation in Asthma." Chest 133, no. 4 (April 2008): 989–98. http://dx.doi.org/10.1378/chest.07-0829.

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Harkins, Michelle. "Therapeutic Targets in Airway Inflammation." Chest 126, no. 5 (November 2004): 1714. http://dx.doi.org/10.1378/chest.126.5.1714.

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Jeffery, P. K. "Bronchial biopsies and airway inflammation." European Respiratory Journal 9, no. 8 (August 1, 1996): 1583–87. http://dx.doi.org/10.1183/09031936.96.09081583.

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Macklem, Peter T. "Functional Consequences of Airway Inflammation." American Review of Respiratory Disease 146, no. 5_pt_1 (November 1992): 1356. http://dx.doi.org/10.1164/ajrccm/146.5_pt_1.1356.

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Wallace, William A. H. "Airway inflammation and the lung." Current Diagnostic Pathology 12, no. 6 (December 2006): 441–50. http://dx.doi.org/10.1016/j.cdip.2006.07.004.

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45

LARSEN, GARY L, and PATRICK G HOLT. "The Concept of Airway Inflammation." American Journal of Respiratory and Critical Care Medicine 162, supplement_1 (August 2000): S2—S6. http://dx.doi.org/10.1164/ajrccm.162.supplement_1.maic-1.

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46

Fabbri, L. M. "Airway Inflammation in Occupational Asthma." American Journal of Respiratory and Critical Care Medicine 150, no. 5_pt_2 (November 1994): S80—S82. http://dx.doi.org/10.1164/ajrccm/150.5_pt_2.s80.

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47

Barbato, Angelo, Graziella Turato, Simonetta Baraldo, Erica Bazzan, Fiorella Calabrese, Maria Tura, Renzo Zuin, et al. "Airway Inflammation in Childhood Asthma." American Journal of Respiratory and Critical Care Medicine 168, no. 7 (October 2003): 798–803. http://dx.doi.org/10.1164/rccm.200305-650oc.

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48

Saglani, Sejal, and Andrew Bush. "Asthma, Atopy, and Airway Inflammation." American Journal of Respiratory and Critical Care Medicine 178, no. 5 (September 2008): 437–38. http://dx.doi.org/10.1164/rccm.200805-796ed.

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49

Merrill, William W., Darryl Carter, and Mark R. Cullen. "The Relationship between Large Airway Inflammation and Airway Metaplasia." Chest 100, no. 1 (July 1991): 131–35. http://dx.doi.org/10.1378/chest.100.1.131.

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50

Saha, Shironjit, and Christopher E. Brightling. "Eosinophilic airway inflammation in COPD." International Journal of COPD 1, no. 1 (January 2006): 39–47. http://dx.doi.org/10.2147/copd.2006.1.1.39.

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Journal articles on the topic 'Airway (Medicine) - Inflammation'

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