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Journal articles on the topic 'Airway remodelling'

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Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

Bergeron, Céline, Meri K. Tulic, and Qutayba Hamid. "Airway Remodelling in Asthma: From Benchside to Clinical Practice." Canadian Respiratory Journal 17, no. 4 (2010): e85-e93. http://dx.doi.org/10.1155/2010/318029.

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Airway remodelling refers to the structural changes that occur in both large and small airways relevant to miscellaneous diseases including asthma. In asthma, airway structural changes include subepithelial fibrosis, increased smooth muscle mass, gland enlargement, neovascularization and epithelial alterations. Although controversial, airway remodelling is commonly attributed to an underlying chronic inflammatory process. These remodelling changes contribute to thickening of airway walls and, consequently, lead to airway narrowing, bronchial hyper-responsiveness, airway edema and mucous hypersecretion. Airway remodelling is associated with poor clinical outcomes among asthmatic patients. Early diagnosis and prevention of airway remodelling has the potential to decrease disease severity, improve control and prevent disease expression. The relationship between structural changes and clinical and functional abnormalities clearly deserves further investigation. The present review briefly describes the characteristic features of airway remodelling observed in asthma, its clinical consequences and relevance for physicians, and its modulation by therapeutic approaches used in the treatment of asthmatic patients.

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2

Kolahian, Saeed, and Reinoud Gosens. "Cholinergic Regulation of Airway Inflammation and Remodelling." Journal of Allergy 2012 (January 16, 2012): 1–9. http://dx.doi.org/10.1155/2012/681258.

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Acetylcholine is the predominant parasympathetic neurotransmitter in the airways that regulates bronchoconstriction and mucus secretion. Recent findings suggest that acetylcholine regulates additional functions in the airways, including inflammation and remodelling during inflammatory airway diseases. Moreover, it has become apparent that acetylcholine is synthesized by nonneuronal cells and tissues, including inflammatory cells and structural cells. In this paper, we will discuss the regulatory role of acetylcholine in inflammation and remodelling in which we will focus on the role of the airway smooth muscle cell as a target cell for acetylcholine that modulates inflammation and remodelling during respiratory diseases such as asthma and COPD.

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3

Royce, Simon G., Anna M. Tominaga, Matthew Shen, Krupesh P. Patel, Brooke M. Huuskes, Rebecca Lim, Sharon D. Ricardo, and Chrishan S. Samuel. "Serelaxin improves the therapeutic efficacy of RXFP1-expressing human amnion epithelial cells in experimental allergic airway disease." Clinical Science 130, no. 23 (October 20, 2016): 2151–65. http://dx.doi.org/10.1042/cs20160328.

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We have identified combination cell-based therapies that effectively treat the airway inflammation and airway remodelling (structural changes) that contribute to airway obstruction and related airway hyperresponsiveness in murine chronic allergic airways.

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4

Chetta, Alfredo, and Dario Olivieri. "Role of Inhaled Steroids in Vascular Airway Remodelling in Asthma and COPD." International Journal of Endocrinology 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/397693.

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In chronic obstructive airway diseases, such as asthma and chronic obstructive pulmonary disease (COPD), changes in bronchial microvasculature are present in response to inflammatory stimuli. Vascular changes may significantly contribute to airway wall remodelling. Angiogenesis and vascular leakage are prevalent in asthma, while vasodilation and vascular leakage dominate in COPD. An endothelial dysfunction may be present both in asthma and in COPD. Vascular changes may occur simultaneously with the thickening of the airway wall and the narrowing of the bronchial lumen. Consequently, pharmacological control of bronchial vascular remodelling may be crucial for symptom control in asthma and COPD. In asthmatic airways, inhaled steroids can downregulate vascular remodelling by acting on proangiogenic factors. Additionally, studies on combination therapy with long-actingβ2-agonists and inhaled steroids have provided evidence of a possible synergistic action on components of vascular remodelling in asthma. In COPD, there is less experimental evidence on the effect of inhaled steroids on airway microvascular changes. Importantly, vascular endothelial growth factor (VEGF), the most specific growth factor for vascular endothelium, is crucially involved in the pathophysiology of airway vascular remodelling, both in asthma and COPD. The inhibition of VEGF and its receptor may be useful in the treatment of the vascular changes in the airway wall.

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5

O'Sullivan, Michael J., Thien-Khoi N. Phung, and Jin-Ah Park. "Bronchoconstriction: a potential missing link in airway remodelling." Open Biology 10, no. 12 (December 2020): 200254. http://dx.doi.org/10.1098/rsob.200254.

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In asthma, progressive structural changes of the airway wall are collectively termed airway remodelling. Despite its deleterious effect on lung function, airway remodelling is incompletely understood. As one of the important causes leading to airway remodelling, here we discuss the significance of mechanical forces that are produced in the narrowed airway during asthma exacerbation, as a driving force of airway remodelling. We cover in vitro , ex vivo and in vivo work in this field, and discuss up-to-date literature supporting the idea that bronchoconstriction may be the missing link in a comprehensive understanding of airway remodelling in asthma.

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6

Royce, Simon G., Amelia Sedjahtera, Chrishan S. Samuel, and Mimi L. K. Tang. "Combination therapy with relaxin and methylprednisolone augments the effects of either treatment alone in inhibiting subepithelial fibrosis in an experimental model of allergic airways disease." Clinical Science 124, no. 1 (September 7, 2012): 41–51. http://dx.doi.org/10.1042/cs20120024.

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Although CSs (corticosteroids) demonstrate potent effects in the control of airway inflammation in asthma, many patients continue to experience symptoms and AHR (airway hyper-responsiveness) despite optimal treatment with these agents, probably due to progressive airway remodelling. Identifying novel therapies that can target airway remodelling and/or airway reactivity may improve symptom control in these patients. We have demonstrated previously that the anti-fibrotic hormone RLN (relaxin) can reverse airway remodelling (epithelial thickening and subepithelial fibrosis) and AHR in a murine model of AAD (allergic airways disease). In the present study, we compared the effects of RLN with a CS (methylprednisolone) on airway remodelling and AHR when administered independently or in combination in the mouse AAD model. Female mice at 6–8 weeks of age were sensitized and challenged to OVA (ovalbumin) over a 9-week period and treated with methylprednisolone, RLN, a combination of both treatments or vehicle controls. Methylprednisolone was administered intraperitoneally on the same day as nebulization for 6 weeks, whereas recombinant human RLN-2 was administered via subcutaneously implanted osmotic mini-pumps from weeks 9–11. RLN or methylprednisolone alone were both able to significantly decrease subepithelial thickness and total lung collagen deposition; whereas RLN but not methylprednisolone significantly decreased epithelial thickness and AHR. Additionally, combination therapy with CS and RLN more effectively reduced subepithelial collagen thickness than either therapy alone. These findings demonstrate that RLN can modulate a broader range of airway remodelling changes and AHR than methylprednisolone and the combination of both treatments offers enhanced control of subepithelial fibrosis.

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7

Wang, Kimberley C. W., Timothy D. Le Cras, Alexander N. Larcombe, Graeme R. Zosky, John G. Elliot, Alan L. James, and Peter B. Noble. "Independent and combined effects of airway remodelling and allergy on airway responsiveness." Clinical Science 132, no. 3 (February 2, 2018): 327–38. http://dx.doi.org/10.1042/cs20171386.

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Airway remodelling and allergic inflammation are key features of airway hyperresponsiveness (AHR) in asthma; however, their interrelationships are unclear. The present study investigated the separate and combined effects of increased airway smooth muscle (ASM) layer thickness and allergy on AHR. We integrated a protocol of ovalbumin (OVA)-induced allergy into a non-inflammatory mouse model of ASM remodelling induced by conditional and airway-specific expression of transforming growth factor-α (TGF-α) in early growth response-1 (Egr-1)-deficient transgenic mice, which produced thickening of the ASM layer following ingestion of doxycycline. Mice were sensitised to OVA and assigned to one of four treatment groups: Allergy – normal chow diet and OVA challenge; Remodelling – doxycycline in chow and saline challenge; Allergy and Remodelling – doxycycline in chow and OVA challenge; and Control – normal chow diet and saline challenge. Airway responsiveness to methacholine (MCh) and histology were assessed. Compared with the Control group, airway responsiveness to MCh was increased in the Allergy group, independent of changes in wall structure, whereas airway responsiveness in the Remodelling group was increased independent of exposure to aeroallergen. The combined effects of allergy and remodelling on airway responsiveness were greater than either of them alone. There was a positive relationship between the thickness of the ASM layer with airway responsiveness, which was shifted upward in the presence of allergy. These findings support allergy and airway remodelling as independent causes of variable and excessive airway narrowing.

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8

Redington. "Fibrosis and airway remodelling." Clinical & Experimental Allergy 30 (June 2000): 42–45. http://dx.doi.org/10.1046/j.1365-2222.2000.00096.x.

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9

Boulet, L.-P., and P. J. Sterk. "Airway remodelling: the future." European Respiratory Journal 30, no. 5 (November 1, 2007): 831–34. http://dx.doi.org/10.1183/09031936.00110107.

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10

Lloyd, C. M., and D. S. Robinson. "Allergen-induced airway remodelling." European Respiratory Journal 29, no. 5 (May 1, 2007): 1020–32. http://dx.doi.org/10.1183/09031936.00150305.

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11

Beasley, R., C. Page, and L. Lichtenstein. "Airway remodelling in asthma." Clinical & Experimental Allergy Reviews 2, no. 4 (July 18, 2002): 109–16. http://dx.doi.org/10.1046/j.1472-9725.2.s4.1.x.

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12

Samitas, Konstantinos, Vasiliki Delimpoura, Eleftherios Zervas, and Mina Gaga. "Anti-IgE treatment, airway inflammation and remodelling in severe allergic asthma: current knowledge and future perspectives." European Respiratory Review 24, no. 138 (November 30, 2015): 594–601. http://dx.doi.org/10.1183/16000617.00001715.

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Asthma is a disorder of the airways involving various inflammatory cells and mediators and characterised by bronchial hyperresponsiveness, chronic inflammation and structural alterations in the airways, also known as remodelling. IgE is an important mediator of allergic reactions and has a central role in allergic asthma pathophysiology, as it is implicated in both the early and late phase allergic response. Moreover, clinical and mechanistic evidence has lately emerged, implicating IgE in the development of airway remodelling. The use of monoclonal antibodies targeting IgE, such as omalizumab, has proven very effective in improving respiratory symptoms and quality of life, while reducing asthma exacerbations, emergency room visits and the use of systemic corticosteroids in allergic severe asthma. These effects are believed to be mainly mediated by omalizumab's inhibitory effect on the initiation and further propagation of the allergic inflammation cascade. However, there is evidence to suggest that anti-IgE treatment remains effective long after it has been discontinued. In part, these findings could be attributed to the possible ameliorating effects of anti-IgE treatment on airway remodelling. In this review, we discuss recent findings supporting the notion that anti-IgE treatment modulates the complex immune responses that manifest clinically as asthma and ameliorates airway remodelling changes often observed in allergic severe asthma phenotypes.

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13

Watelet, J. B., T. Van Zele, M. Gjomarkaj, G. W. Canonica, S. E. Dahlen, W. Fokkens, V. J. Lund, et al. "Tissue remodelling in upper airways: where is the link with lower airway remodelling?" Allergy 61, no. 11 (November 2006): 1249–58. http://dx.doi.org/10.1111/j.1398-9995.2006.01226.x.

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14

Riccioni, G., N. D'Orazio, R. Della Vecchia, T. Iezzi, and C. Di Ilio. "Remodelling and Inflammation in Bronchial Asthma." European Journal of Inflammation 1, no. 1 (January 2003): 9–12. http://dx.doi.org/10.1177/1721727x0300100103.

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Chronic stable asthma is characterized by inflammation of the airway wall, with abnormal accumulation of basophils, eosinophils, lymphocytes, mast cells, macrophages, dendritic cells and myofibroblasts. The airway inflammation is not confined to severe asthma, but is also found in mild and moderate asthma. This inflammation results in a peculiar type of lymphocytic infiltration whereby Th2 lymphocytes secrete cytokines that orchestrate cellular inflammation and promote airway hyperresponsiveness. The term “airway remodelling” in bronchial asthma refers to structural changes that occurr in conjunction with, or because of, chronic airway inflammation. Airway remodelling results in alterations in the airway epithelium, lamina propria, and submucosa, leading to thickening of airway wall. The consequences of airway remodelling in asthma include incompletely reversible airway narrowing, bronchial hyperresponsiveness (BHR), smooth muscle contraction, airway edema, and mucus hypersecretion which may predispose persons with asthma to exacerbations and even death from airway obstruction.

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15

Dournes, Gaël, and François Laurent. "Airway Remodelling in Asthma and COPD: Findings, Similarities, and Differences Using Quantitative CT." Pulmonary Medicine 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/670414.

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Airway remodelling is a well-established feature in asthma and chronic obstructive lung disease (COPD), secondary to chronic airway inflammation. The structural changes found on pathological examination of remodelled airway wall have been shown to display similarities but also differences. Computed tomography (CT) is today a remarkable tool to assess airway wall morphologyin vivosince submillimetric acquisitions over the whole lung volume could be obtained allowing 3D evaluation. Recently, CT-derived indices extracted from CT images have been described and are thought to assess airway remodelling. This may help understand the complex mechanism underlying the remodelling process, which is still not fully understood. This paper summarizes the various methods described to quantify airway remodelling in asthma and COPD using CT, and similarities and differences between both diseases will be emphasized.

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16

Dilasser, Florian, Lindsay Rose, Dorian Hassoun, Martin Klein, Morgane Rousselle, Carole Brosseau, Christophe Guignabert, et al. "Essential role of smooth muscle Rac1 in severe asthma-associated airway remodelling." Thorax 76, no. 4 (February 4, 2021): 326–34. http://dx.doi.org/10.1136/thoraxjnl-2020-216271.

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BackgroundSevere asthma is a chronic lung disease characterised by inflammation, airway hyperresponsiveness (AHR) and airway remodelling. The molecular mechanisms underlying uncontrolled airway smooth muscle cell (aSMC) proliferation involved in pulmonary remodelling are still largely unknown. Small G proteins of the Rho family (RhoA, Rac1 and Cdc42) are key regulators of smooth muscle functions and we recently demonstrated that Rac1 is activated in aSMC from allergic mice. The objective of this study was to assess the role of Rac1 in severe asthma-associated airway remodelling.Methods and resultsImmunofluorescence analysis in human bronchial biopsies revealed an increased Rac1 activity in aSMC from patients with severe asthma compared with control subjects. Inhibition of Rac1 by EHT1864 showed that Rac1 signalling controlled human aSMC proliferation induced by mitogenic stimuli through the signal transducer and activator of transcription 3 (STAT3) signalling pathway. In vivo, specific deletion of Rac1 in SMC or pharmacological inhibition of Rac1 by nebulisation of NSC23766 prevented AHR and aSMC hyperplasia in a mouse model of severe asthma. Moreover, the Rac1 inhibitor prevented goblet cell hyperplasia and epithelial cell hypertrophy whereas treatment with corticosteroids had less effect. Nebulisation of NSC23766 also decreased eosinophil accumulation in the bronchoalveolar lavage of asthmatic mice.ConclusionThis study demonstrates that Rac1 is overactive in the airways of patients with severe asthma and is essential for aSMC proliferation. It also provides evidence that Rac1 is causally involved in AHR and airway remodelling. Rac1 may represent as an interesting target for treating both AHR and airway remodelling of patients with severe asthma.

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17

RAMSAY, Scott G., Christopher J. KENYON, Niall WHYTE, Ian C. MCKAY, Neil C. THOMSON, and George B. M. LINDOP. "Effects of angiotensin II on remodelling of the airway and the vasculature in the rat." Clinical Science 98, no. 1 (November 19, 1999): 1–7. http://dx.doi.org/10.1042/cs0980001.

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Airway remodelling occurs in chronic asthma. Angiotensin II promotes growth in cardiovascular remodelling. Since the renin–angiotensin system is activated in acute severe asthma, we hypothesized that angiotensin II has a role in airway remodelling. A total of 14 young male Wistar rats were randomly divided into two groups. All received 2-week infusions of bromodeoxyuridine, and the experimental group also received angiotensin II. Blood pressure rose in the angiotensin II-infused group [mean levels: pre-infusion, 134.9 (S.D. 14.7) mmHg; post-infusion, 197.1 (22.5) mmHg], and expression of renin mRNA in the renal juxtaglomerular cells was suppressed in these animals. The proportion of bromodeoxyuridine-positive cell nuclei was no different in the airways of control and angiotensin II-infused animals for smooth muscle [mean bromodeoxyuridine index: control, 8.6% (S.E.M. 1.1%); angiotensin II, 9.3% (1.1%)], epithelium [control, 16.7% (2.3%); angiotensin II, 16.0% (2.2%)] and adventitia [control, 26.4% (2.2%); angiotensin II, 26.6% (2.4%)]. In the arteries, bromodeoxyuridine indices were higher in the angiotensin II-infused rats [18.4% (2.3%)] than in the control animals [9.4% (2.8%)], but no difference was found in the veins [12% (2.9%) and 11.4% (2.6%) respectively]. Morphometry of the airway wall and mesenteric vasculature was no different in the two groups. Therefore a 2-week infusion of angiotensin II increases blood pressure and DNA synthesis in the mesenteric arteries, but does not cause airway remodelling, in the rat.

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18

James, A. L., and S. Wenzel. "Clinical relevance of airway remodelling in airway diseases." European Respiratory Journal 30, no. 1 (March 14, 2007): 134–55. http://dx.doi.org/10.1183/09031936.00146905.

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19

Redington, A. E., and P. H. Howarth. "Airway wall remodelling in asthma." Thorax 52, no. 4 (April 1, 1997): 310–12. http://dx.doi.org/10.1136/thx.52.4.310.

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20

Westergren-Thorsson, Gunilla, Kristoffer Larsen, Kristian Nihlberg, Annika Andersson-Sjöland, Oskar Hallgren, György Marko-Varga, and Leif Bjermer. "Pathological airway remodelling in inflammation." Clinical Respiratory Journal 4 (May 2010): 1–8. http://dx.doi.org/10.1111/j.1752-699x.2010.00190.x.

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21

Okayama, Y., S. Okumura, N. Yamashita, K. Ohta, and H. Saito. "Mast cell-mediated airway remodelling." Clinical Experimental Allergy Reviews 6, no. 4 (June 2006): 80–84. http://dx.doi.org/10.1111/j.1365-2222.2006.00105.x.

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22

Lindén, Anders. "Interleukin-17 and airway remodelling." Pulmonary Pharmacology & Therapeutics 19, no. 1 (February 2006): 47–50. http://dx.doi.org/10.1016/j.pupt.2005.02.004.

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23

Lloyd, Clare M., Douglas S. Robinson, and Sarah J. McMillan. "Modelling airway remodelling in asthma." Drug Discovery Today: Disease Models 1, no. 4 (December 2004): 425–30. http://dx.doi.org/10.1016/j.ddmod.2004.11.013.

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24

Ramos-Ramírez, Patricia, Jielu Liu, Sofia Mogren, Joshua Gregory, Malin Noreby, Anne Petrén, Ying Lei, et al. "House Dust Mite and Cat Dander Extract Induce Asthma-Like Histopathology with an Increase of Mucosal Mast Cells in a Guinea Pig Model." Journal of Immunology Research 2023 (January 31, 2023): 1–10. http://dx.doi.org/10.1155/2023/9393497.

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Background. Asthma is a chronic inflammatory disease with structural changes in the lungs defined as airway remodelling. Mast cell responses are important in asthma as they, upon activation, release mediators inducing bronchoconstriction, inflammatory cell recruitment, and often remodelling of the airways. As guinea pigs exhibit anatomical, physiological, and pharmacological features resembling human airways, including mast cell distribution and mediator release, we evaluated the effect of extracts from two common allergens, house dust mite (HDM) and cat dander (CDE), on histopathological changes and the composition of tryptase- and chymase-positive mast cells in the guinea pig lungs. Methods. Guinea pigs were exposed intranasally to HDM or CDE for 4, 8, and 12 weeks, and airway histology was examined at each time point. Hematoxylin and eosin, Picro-Sirius Red, and Periodic Acid-Schiff staining were performed to evaluate airway inflammation, collagen deposition, and mucus-producing cells. In addition, Astra blue and immunostaining against tryptase and chymase were used to visualize mast cells. Results. Repetitive administration of HDM or CDE led to the accumulation of inflammatory cells into the proximal and distal airways as well as increased airway smooth muscle mass. HDM exposure caused subepithelial collagen deposition and mucus cell hyperplasia at all three time points, whereas CDE exposure only caused these effects at 8 and 12 weeks. Both HDM and CDE induced a substantial increase in mast cells after 8 and 12 weeks of challenges. This increase was primarily due to mast cells expressing tryptase, but not chymase, thus indicating mucosal mast cells. Conclusions. We here show that exposure to HDM and CDE elicits asthma-like histopathology in guinea pigs with infiltration of inflammatory cells, airway remodelling, and accumulation of primarily mucosal mast cells. The results together encourage the use of HDM and CDE allergens for the stimulation of a clinically relevant asthma model in guinea pigs.

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Berair, Rachid, Ruth Hartley, Vijay Mistry, Ajay Sheshadri, Sumit Gupta, Amisha Singapuri, Sherif Gonem, et al. "Associations in asthma between quantitative computed tomography and bronchial biopsy-derived airway remodelling." European Respiratory Journal 49, no. 5 (May 2017): 1601507. http://dx.doi.org/10.1183/13993003.01507-2016.

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Airway remodelling in asthma remains poorly understood. This study aimed to determine the association of airway remodelling measured on bronchial biopsies with 1) lung function impairment and 2) thoracic quantitative computed tomography (QCT)-derived morphometry and densitometry measures of proximal airway remodelling and air trapping.Subjects were recruited from a single centre. Bronchial biopsy remodelling features that were the strongest predictors of lung function impairment and QCT-derived proximal airway morphometry and air trapping markers were determined by stepwise multiple regression. The best predictor of air trapping was validated in an independent replication group.Airway smooth muscle % was the only predictor of post-bronchodilator forced expiratory volume in 1 s (FEV1) % pred, while both airway smooth muscle % and vascularity were predictors of FEV1/forced vital capacity. Epithelial thickness and airway smooth muscle % were predictors of mean segmental bronchial luminal area (R2=0.12; p=0.02 and R2=0.12; p=0.015), whereas epithelial thickness was the only predictor of wall area % (R2=0.13; p=0.018). Vascularity was the only significant predictor of air trapping (R2=0.24; p=0.001), which was validated in the replication group (R2=0.19; p=0.031).In asthma, airway smooth muscle content and vascularity were both associated with airflow obstruction. QCT-derived proximal airway morphometry was most strongly associated with epithelial thickness and airway smooth muscle content, whereas air trapping was related to vascularity.

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GABAZZA, Esteban C., Osamu TAGUCHI, Shigenori TAMAKI, Shuichi MURASHIMA, Hiroyasu KOBAYASHI, Hiroki YASUI, Tetsu KOBAYASHI, Osamu HATAJI, and Yukihiko ADACHI. "Role of nitric oxide in airway remodelling." Clinical Science 98, no. 3 (February 9, 2000): 291–94. http://dx.doi.org/10.1042/cs0980291.

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Airway remodelling, which is manifested by thickening of bronchial wall, is an important causative factor of bronchial hyper-responsiveness in asthma. The pathophysiological mechanism of airway remodelling is not clear. In the present study we evaluated the relationship between nitric oxide (NO) generation and airway wall thickening in patients with chronic asthma. As a marker of NO production, the levels of nitrite/nitrate were measured in induced sputum, and bronchial wall thickening was measured by high-resolution computed tomography. Sputum concentrations of nitrite/nitrate were significantly increased in asthmatic patients compared with controls. The ratio of airway wall thickness to lumen diameter was significantly correlated with the sputum concentration of nitrite/nitrate. Although statistical correlation does not prove causation, this finding suggests that NO may play a key role in the pathogenesis of airway remodelling.

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Germain, Adeline, Jeanne-Marie Perotin, Gonzague Delepine, Myriam Polette, Gaëtan Deslée, and Valérian Dormoy. "Whole-Exome Sequencing of Bronchial Epithelial Cells Reveals a Genetic Print of Airway Remodelling in COPD." Biomedicines 10, no. 7 (July 15, 2022): 1714. http://dx.doi.org/10.3390/biomedicines10071714.

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The remodelling of the airways is a hallmark of chronic obstructive pulmonary disease, but it is highly heterogeneous and erratically distributed in the airways. To assess the genetic print of remodelling in chronic obstructive pulmonary disease (COPD), we performed a comparative whole-exome sequencing analysis on microdissected bronchial epithelia. Lung resections from four non-COPD and three COPD subjects (ex-smokers and current smokers) were formalin-fixed paraffin-embedded (FFPE). Non-remodelled and remodelled bronchial epithelia were isolated by laser microdissection. Genomic DNA was captured and sequenced. The comparative quantitative analysis identified a list of 109 genes as having variants in remodelled epithelia and 160 genes as having copy number alterations in remodelled epithelia, mainly in COPD patients. The functional analysis highlighted cilia-associated processes. Therefore, bronchial-remodelled epithelia appeared genetically more altered than non-remodelled epithelia. Characterizing the unique molecular print of airway remodelling in respiratory diseases may help uncover additional factors contributing to epithelial dysfunctions, ultimately providing additional targetable proteins to correct epithelial remodelling and improve lung function.

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Laprise, C., M. Laviolette, M. Boutet, and L. Boulet. "Asymptomatic airway hyperresponsiveness: relationships with airway inflammation and remodelling." European Respiratory Journal 14, no. 1 (July 1999): 63. http://dx.doi.org/10.1034/j.1399-3003.1999.14a12.x.

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Wang, Yujie, Man Jia, Xiaoyi Yan, Limin Cao, Peter J. Barnes, Ian M. Adcock, Mao Huang, and Xin Yao. "Increased neutrophil gelatinase-associated lipocalin (NGAL) promotes airway remodelling in chronic obstructive pulmonary disease." Clinical Science 131, no. 11 (May 22, 2017): 1147–59. http://dx.doi.org/10.1042/cs20170096.

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Airway remodelling is an important component of chronic obstructive pulmonary disease (COPD). Neutrophil gelatinase-associated lipocalin (NGAL) from neutrophils may drive COPD epithelial–mesenchymal transition (EMT). NGAL expression was quantified in the lungs of COPD patients and bronchoalveolar lavage fluid (BALF) of ozone-treated mice. Reticular basement membrane (RBM) thickness and E-cadherin and α-smooth muscle actin (α-SMA) expression were determined in mice airways. Effects of cigarette smoke extract (CSE) and inflammatory factors on NGAL expression in human neutrophils as well as the effects of NGAL on airway structural cells was assessed. NGAL was mainly distributed in neutrophils and enhanced in lung tissues of both COPD patients and BALF of ozone-treated mice. We showed decreased E-cadherin and increased α-SMA expression in bronchial epithelium and increased RBM thickness in ozone-treated animals. In vitro, CSE, IL-1β and IL-17 enhanced NGAL mRNA expression in human neutrophils. NGAL, in turn, down-regulated the expression of E-cadherin and up-regulated α-SMA expression in 16HBE cells via the WNT/glycogensynthase kinase-3β (GSK-3β) pathway. Furthermore, NGAL promoted the proliferation and migration of human bronchial smooth muscle cells (HASMCs). The present study suggests that elevated NGAL promotes COPD airway remodelling possibly through altered EMT. NGAL may be a potential target for reversing airway obstruction and remodelling in COPD.

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Mainguy-Seers, Sophie, Amandine Vargas, Olivia Labrecque, Christian Bédard, Pierre Hélie, and Jean-Pierre Lavoie. "Randomised study of the immunomodulatory effects of azithromycin in severely asthmatic horses." Veterinary Record 185, no. 5 (August 1, 2019): 143. http://dx.doi.org/10.1136/vr.105260.

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Neutrophilic inflammation is believed to contribute to the airway obstruction and remodelling in equine asthma. Azithromycin, an antibiotic with immunomodulatory properties, reduces pulmonary neutrophilia and hyper-responsiveness in human asthmatics and decreases airway remodelling in rodent models of asthma. It was therefore hypothesised that azithromycin would improve lung function, mucus accumulation and central airway remodelling by decreasing luminal neutrophilia in severe equine asthma. The effects of a 10-day treatment with either azithromycin or ceftiofur, an antimicrobial without immune-modulating activity, were assessed using a blind, randomised, crossover design with six severe asthmatic horses in clinical exacerbation. Lung function, tracheal mucus accumulation, tracheal wash bacteriology, bronchial remodelling, airway neutrophilia and mRNA expression of proinflammatory cytokines (interleukin (IL)-8, IL-17A, IL-1β, tumour necrosis factor-α) in bronchoalveolar lavage fluid were evaluated. Azithromycin decreased the expression of IL-8 (P=0.03, one-tailed) and IL-1β (P=0.047, one-tailed) but failed to improve the other variables evaluated. Ceftiofur had no effect on any parameter. The reduction of neutrophilic chemoattractants (IL-8, IL-1β) justifies further efforts to investigate the effects of a prolonged treatment with macrolides on airway neutrophilia and remodelling. The lack of efficacy of ceftiofur suggests that severe equine asthma should not be treated with antibiotics at first-line therapy.

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Royce, S. G., C. X. F. Lim, K. P. Patel, B. Wang, C. S. Samuel, and M. L. K. Tang. "Intranasally administered serelaxin abrogates airway remodelling and attenuates airway hyperresponsiveness in allergic airways disease." Clinical & Experimental Allergy 44, no. 11 (October 21, 2014): 1399–408. http://dx.doi.org/10.1111/cea.12391.

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Wilson. "What causes airway remodelling in asthma?" Clinical & Experimental Allergy 28, no. 5 (May 1998): 534–36. http://dx.doi.org/10.1046/j.1365-2222.1998.00298.x.

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Boulet, L.-P., and P. J. Sterk. "A new series on airway remodelling." European Respiratory Journal 29, no. 2 (September 27, 2006): 231–32. http://dx.doi.org/10.1183/09031936.00132406.

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Zimmerman, P. "Discussion session III: Airway wall remodelling." Clinical & Experimental Allergy Reviews 1, no. 2 (July 2001): 123–27. http://dx.doi.org/10.1046/j.1472-9725.2001.00022.x.

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Kuehnel, Mark, Lavinia Maegel, Jens Vogel-Claussen, Jan Lukas Robertus, and Danny Jonigk. "Airway remodelling in the transplanted lung." Cell and Tissue Research 367, no. 3 (November 12, 2016): 663–75. http://dx.doi.org/10.1007/s00441-016-2529-0.

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Niimi, Akio, Hisako Matsumoto, Masayoshi Minakuchi, Masanori Kitaichi, and Ryoichi Amitani. "Airway remodelling in cough-variant asthma." Lancet 356, no. 9229 (August 2000): 564–65. http://dx.doi.org/10.1016/s0140-6736(00)02584-8.

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Beckett, P. A. "Pharmacotherapy and airway remodelling in asthma?" Thorax 58, no. 2 (February 1, 2003): 163–74. http://dx.doi.org/10.1136/thorax.58.2.163.

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Saglani, Sejal, and Clare M. Lloyd. "Novel concepts in airway inflammation and remodelling in asthma." European Respiratory Journal 46, no. 6 (November 5, 2015): 1796–804. http://dx.doi.org/10.1183/13993003.01196-2014.

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The hallmark pathological features of asthma include airway eosinophilic inflammation and structural changes (remodelling) which are associated with an irreversible loss in lung function that tracks from childhood to adulthood. In parallel with changes in function, pathological abnormalities occur early, during the pre-school years, are established by school age and subsequently remain (even though symptoms may remit for periods during adulthood). Given the equal importance of inflammation and remodelling in asthma pathogenesis, there is a significant disparity in studies undertaken to investigate the contribution of each. The majority focus on the role of inflammation, and although novel therapeutics such as those targeted against T-helper cell type 2 (Th2) mediators have arisen, it is apparent that targeting inflammation alone has not allowed disease modification. Therefore, unless airway remodelling is addressed for future therapeutic strategies, it is unlikely that we will progress towards a cure for asthma. Having acknowledged these limitations, the focus of this review is to highlight the gaps in our current knowledge about the mechanisms underlying airway remodelling, the relationships between remodelling, inflammation and function, remodelling and clinical phenotypes, and the importance of utilising innovative and realistic pre-clinical models to uncover effective, disease-modifying therapeutic strategies.

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Namvar, Sara, Briony Labram, Jessica Rowley, and Sarah Herrick. "Aspergillus fumigatus—Host Interactions Mediating Airway Wall Remodelling in Asthma." Journal of Fungi 8, no. 2 (February 6, 2022): 159. http://dx.doi.org/10.3390/jof8020159.

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Asthma is a chronic heterogeneous respiratory condition that is mainly associated with sensitivity to airborne agents such as pollen, dust mite products and fungi. Key pathological features include increased airway inflammation and airway wall remodelling. In particular, goblet cell hyperplasia, combined with excess mucus secretion, impairs clearance of the inhaled foreign material. Furthermore, structural changes such as subepithelial fibrosis and increased smooth muscle hypertrophy collectively contribute to deteriorating airway function and possibility of exacerbations. Current pharmacological therapies focused on airway wall remodelling are limited, and as such, are an area of unmet clinical need. Sensitisation to the fungus, Aspergillus fumigatus, is associated with enhanced asthma severity, bronchiectasis, and hospitalisation. How Aspergillus fumigatus may drive airway structural changes is unclear, although recent evidence points to a central role of the airway epithelium. This review provides an overview of the airway pathology in patients with asthma and fungal sensitisation, summarises proposed airway epithelial cell–fungal interactions and discusses the initiation of a tissue remodelling response. Related findings from in vivo animal models are included given the limited analysis of airway pathology in patients. Lastly, an important role for Aspergillus fumigatus-derived proteases in triggering a cascade of damage-repair events through upregulation of airway epithelial-derived factors is proposed.

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Karakioulaki, Meropi, Eleni Papakonstantinou, and Daiana Stolz. "Extracellular matrix remodelling in COPD." European Respiratory Review 29, no. 158 (November 18, 2020): 190124. http://dx.doi.org/10.1183/16000617.0124-2019.

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The extracellular matrix (ECM) of the lung plays several important roles in lung function, as it offers a low resistant pathway that allows the exchange of gases, provides compressive strength and elasticity that supports the fragile alveolar–capillary intersection, controls the binding of cells with growth factors and cell surface receptors and acts as a buffer against retention of water.COPD is a chronic inflammatory respiratory condition, characterised by various conditions that result in progressive airflow limitation. At any stage in the course of the disease, acute exacerbations of COPD may occur and lead to accelerated deterioration of pulmonary function. A key factor of COPD is airway remodelling, which refers to the serious alterations of the ECM affecting airway wall thickness, resistance and elasticity. Various studies have shown that serum biomarkers of ECM turnover are significantly associated with disease severity in patients with COPD and may serve as potential targets to control airway inflammation and remodelling in COPD. Unravelling the complete molecular composition of the ECM in the diseased lungs will help to identify novel biomarkers for disease progression and therapy.

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Vitenberga, Zane, Māra Pilmane, and Aurika Babjoniševa. "COPD affected lung tissue remodelling due to the local distribution of MMP-2, TIMP-2, TGF-β1 and HSP-70." Papers on Anthropology 26, no. 2 (September 18, 2017): 157. http://dx.doi.org/10.12697/poa.2017.26.2.16.

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Chronic obstructive pulmonary disease (COPD) is strongly associated with progressive airway limitation where the key mechanism is abnormal airway remodelling of bronchial mucosa maintained by complex crosstalk of tissue remodelling and regulatory factors. The aim of this study was to determine the appearance and local distribution of tissue remodelling factors in COPD-affected lung tissue and to compare the findings with the control group. In this study, lung tissue specimens were obtained from 27 patients with COPD and 49 control patients. Tissue samples were examined by routine hematoxylin and eosin staining. Remodelling and regulatory factors matrix metalloproteinase-2 (MMP-2), tissue inhibitor of metalloproteinase-2 (TIMP-2), transforming growth factor-β1 (TGF-β1), as well as heat shock protein-70 (Hsp-70) were detected by immunohistochemistry in airway mucosa. The numbers of positive structures were evaluated semiquantitatively. Non-parametrical statistical analysis was performed. Overall COPD-affected lung tissue presented chronic inflammation and tissue remodelling in routine histological analysis. Compared to the control group, statistically significant (P<0.05) difference was calculated between COPD-affected lung tissue and control group with overall more immunoreactive cells containing MMP-2, TIMP-2 and TGF-β1 and less Hsp-70 immunoreactive bronchial epithelial cells, subepithelial connective tissue fibroblasts, bronchial smooth muscle cells and secretory cells of bronchial glands with more pronounced findings of TGF-β1, however, less Hsp-70. Study findings suggest pronounced tissue damage and remodelling with the local regulatory environment of up-regulated TGF-β1. Increased numbers of MMP-2, TIMP-2 and TGF-β1 immunoreactive cells suggest the key role of these remodelling factors in COPD pathogenesis. Decrease of Hsp-70 proves increased cell damage in COPD-affected airway mucosa.

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Ozier, Annaïg, Benoit Allard, Imane Bara, Pierre-Olivier Girodet, Thomas Trian, Roger Marthan, and Patrick Berger. "The Pivotal Role of Airway Smooth Muscle in Asthma Pathophysiology." Journal of Allergy 2011 (December 11, 2011): 1–20. http://dx.doi.org/10.1155/2011/742710.

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Asthma is characterized by the association of airway hyperresponsiveness (AHR), inflammation, and remodelling. The aim of the present article is to review the pivotal role of airway smooth muscle (ASM) in the pathophysiology of asthma. ASM is the main effector of AHR. The mechanisms of AHR in asthma may involve a larger release of contractile mediators and/or a lower release of relaxant mediators, an improved ASM cell excitation/contraction coupling, and/or an alteration in the contraction/load coupling. Beyond its contractile function, ASM is also involved in bronchial inflammation and remodelling. Whereas ASM is a target of the inflammatory process, it can also display proinflammatory and immunomodulatory functions, through its synthetic properties and the expression of a wide range of cell surface molecules. ASM remodelling represents a key feature of asthmatic bronchial remodelling. ASM also plays a role in promoting complementary airway structural alterations, in particular by its synthetic function.

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Stewart, Alastair G. "Airway Wall Remodelling and Hyperresponsiveness: Modelling Remodelling in Vitro and in Vivo." Pulmonary Pharmacology & Therapeutics 14, no. 3 (June 2001): 255–65. http://dx.doi.org/10.1006/pupt.2001.0290.

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Gosens, Reinoud, and Nicholas Gross. "The mode of action of anticholinergics in asthma." European Respiratory Journal 52, no. 4 (August 16, 2018): 1701247. http://dx.doi.org/10.1183/13993003.01247-2017.

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Acetylcholine binds to muscarinic receptors to play a key role in the pathophysiology of asthma, leading to bronchoconstriction, increased mucus secretion, inflammation and airway remodelling. Anticholinergics are muscarinic receptor antagonists that are used in the treatment of chronic obstructive pulmonary disease and asthma. Recent in vivo and in vitro data have increased our understanding of how acetylcholine contributes to the disease manifestations of asthma, as well as elucidating the mechanism of action of anticholinergics. This review assesses the latest literature on acetylcholine in asthma pathophysiology, with a closer look at its role in airway inflammation and remodelling. New insights into the mechanism of action of anticholinergics, their effects on airway remodelling, and a review of the efficacy and safety of long-acting anticholinergics in asthma treatment will also be covered, including a summary of the latest clinical trial data.

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Hardy, Charles Linton, Hong-An Nguyen, Jun Yao, David M. De Kretser, Jennifer M. Rolland, Gary P. Anderson, David J. Phillips, and Robyn E. O’Hehir. "Follistatin is a candidate endogenous negative regulator of activin A in experimental allergic asthma (39.7)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S26. http://dx.doi.org/10.4049/jimmunol.178.supp.39.7.

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Abstract Background: Activin A is a member of the TGF-β superfamily implicated in asthmatic inflammation and tissue remodelling. In vitro, activin A bioactivity is neutralized by the soluble binding protein follistatin. Objective: To determine the potential of endogenous follistatin to suppress activin A in vivo by analysing their relative tissue and kinetic compartmentalization in acute and chronic allergic airway inflammation. Methods: Ovalbumin-sensitized mice were subjected to acute or chronic allergen challenge protocols. Kinetics and distribution of activin A and follistatin were measured in lung tissue and BAL in relation to airway eosinophilia, Th2 cytokines, mucus production and collagen deposition. Results: In both models peak BAL activin A and follistatin concentrations coincided with maximal airway eosinophilia, and frequency of IL-4, IL-5 and IL-13 producing cells in draining lymph nodes; follistatin and activin A immunoreactivity were lost in airway epithelium in parallel with goblet cell metaplasia. In the chronic model inflammation preceded remodelling associated with elevated BAL activin A and TGF-β. Exogenous follistatin inhibited acute allergic airway inflammation. Conclusion: Follistatin is preformed in the normal lung and released in concert with activin A suggesting it serves as an endogenous regulator. Follistatin has potential as a therapeutic to limit airway remodelling.

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Chiappara, Giuseppina, Rosalia Gagliardo, Antonella Siena, Maria Rosaria Bonsignore, Jean Bousquet, Giovanni Bonsignore, and Antonio M. Vignola. "Airway remodelling in the pathogenesis of asthma." Current Opinion in Allergy and Clinical Immunology 1, no. 1 (February 1, 2001): 85–93. http://dx.doi.org/10.1097/01.all.0000010990.97765.a1.

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Venge, Per. "The eosinophil and airway remodelling in asthma." Clinical Respiratory Journal 4 (May 2010): 15–19. http://dx.doi.org/10.1111/j.1752-699x.2010.00192.x.

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Lee, Heung-Man. "Tissue remodelling in upper airway; epigenetic regulation." Nihon Bika Gakkai Kaishi (Japanese Journal of Rhinology) 55, no. 1 (2016): 62. http://dx.doi.org/10.7248/jjrhi.55.62.

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Holgate, S. T. "What does inflammation and airway remodelling mean?" Clinical & Experimental Allergy Reviews 1, no. 2 (July 2001): 59–61. http://dx.doi.org/10.1046/j.1472-9725.2001.00006.x.

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Kariyawasam, H. H., and D. S. Robinson. "Airway remodelling in asthma: models and supermodels?" Clinical Experimental Allergy 35, no. 2 (February 2005): 117–21. http://dx.doi.org/10.1111/j.1365-2222.2005.02173.x.

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