Relevant bibliographies by topics / Airway inflammation

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Airway inflammation'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 July 2025

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Journal articles on the topic "Airway inflammation"

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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 (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
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Boulet, Louis-Philippe, Jamila Chakir, Jean Dubé, Catherine Laprise, Michel Boutet, and Michel Laviolette. "Airway Inflammation and Structural Changes in Airway Hyper-Responsiveness and Asthma: An Overview." Canadian Respiratory Journal 5, no. 1 (1998): 16–21. http://dx.doi.org/10.1155/1998/926439.

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Asthma treatment has moved from bronchodilator therapy to an emphasis on anti-inflammatory therapy. Airway inflammation is believed to induce airway hyper-responsiveness (AHR) through the release of mediators that increase the airway response to agonists. However, the exact contribution of airway inflammation in the physiology of airway hyper-responsiveness remains undefined. Structural modifications in airways resulting from inflammation may contribute to the development and persistence of AHR and the development of asthma. This paper reviews some of the main components of airway inflammation
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O'Byrne, Paul M. "Airway Inflammation and the Pathogenesis of Asthma." Canadian Respiratory Journal 1, no. 3 (1994): 189–95. http://dx.doi.org/10.1155/1994/767528.

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Airway inflammation has been recognized for more than l00 years to be present in the airways of patients with severe asthma. Much more recently, airway intlammation has been identified to be central to the pathogenesis of all asthma. The inflammation is of a characteristic type, with the presence of activated eosinophils, mast cells and lymphocytes in bronchoalveolar lavage fluid and airway biopsies from patients with even mild asthma. Stimuli that are known to worsen asthma, such as inhaled allergens, also increase the numbers of mast cells and cosinophils in asthmatic airways. In addition, t
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Zimmermann, Nives, Marc Rothenberg, and Leah Kottyan. "IL-13 is required and sufficient for airway acidification in allergic airway inflammation (141.16)." Journal of Immunology 184, no. 1_Supplement (2010): 141.16. http://dx.doi.org/10.4049/jimmunol.184.supp.141.16.

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Abstract Clinical studies have shown acidification of airways in asthma. Importantly, studies have suggested that acidification contributes to the pathophysiological process. However, the mechanism of acidification is unclear. We developed a novel method for measuring the acidity of mouse airways and demonstrated that mouse airways are acidified during models of allergic airway inflammation. Our studies determined that airway acidification does not develop in IL-13-deficient mice and that IL-13 delivery alone is sufficient to induce airway acidification. There are multiple ways IL-13 could lea
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Takahashi, Kentaro, Koichi Hirose, Saki Kawashima, et al. "IL-22 attenuates IL-25 production by lung epithelial cells and inhibits antigen-induced eosinophilic airway inflammation (59.8)." Journal of Immunology 188, no. 1_Supplement (2012): 59.8. http://dx.doi.org/10.4049/jimmunol.188.supp.59.8.

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Abstract BACKGROUND: IL-22 functions as both a proinflammatory and an anti-inflammatory cytokine in various inflammations. However, the roles of IL-22 in the allergic airway inflammation are still largely unknown. OBJECTIVE: We sought to determine whether IL-22 is involved in the regulation of allergic airway inflammation. METHODS: We examined IL-22 production and its cellular source at the site of antigen-induced airway inflammation in mice. We also examined the effect of IL-22 neutralization, as well as IL-22 administration. We finally examined the effect of IL-22 on IL-25 production from a
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Shelhamer, James H. "Airway Inflammation." Annals of Internal Medicine 123, no. 4 (1995): 288. http://dx.doi.org/10.7326/0003-4819-123-4-199508150-00008.

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Royce, Simon G., Anna M. Tominaga, Matthew Shen, et al. "Serelaxin improves the therapeutic efficacy of RXFP1-expressing human amnion epithelial cells in experimental allergic airway disease." Clinical Science 130, no. 23 (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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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 (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
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O’Byrne, Paul M. "Airway Inflammation and Airway Hyperresponsiveness." Chest 90, no. 4 (1986): 575–77. http://dx.doi.org/10.1378/chest.90.4.575.

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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 air
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Dissertations / Theses on the topic "Airway inflammation"

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Zhao, Jingyue. "Th17 responses in airway inflammation and airway remodelling." Thesis, King's College London (University of London), 2011. http://kclpure.kcl.ac.uk/portal/en/theses/th17-responses-in-airway-inflammation-and-airway-remodelling(94ca2e63-6304-4694-998e-b40747ca0f9a).html.

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Liu, Jia Clinical School Prince of Wales Hospital Faculty of Medicine UNSW. "Nitric oxide in airway inflammation." Publisher:University of New South Wales. Clinical School - Prince of Wales Hospital, 2009. http://handle.unsw.edu.au/1959.4/43678.

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Exhaled breath condensate (EBC) is a non-invasive method of investigating airway inflammation associated with nitric oxide (NO) and the metabolites nitrite/nitrates (NOx) in diseases such as chronic obstructive pulmonary disease (COPD), but some of the variables affecting the results are unknown. It was hypothesised that 1) EBC would be influenced by lung volumes and the type of EBC collection device; 2) fractional exhaled NO (FENO) and EBC NOx in COPD patients would be altered by smoking and glucocorticosteroids (GCS); 3) cigarette smoke could contribute to the EBC NOx concentration while it
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Mulrennan, Siobhain A. "Diagnosis and treatment in airway inflammation." Thesis, University of Hull, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441682.

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Siva, Roshan. "Modulation of airway inflammation in COPD." Thesis, University of Leicester, 2006. http://hdl.handle.net/2381/4732.

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Inflammation in foregut derivatives outside the lung may contribute to amplification of airway inflammation. I have shown that a management strategy aiming to minimise eosinophilic airway inflammation as well as symptoms is associated with a significant 62% reduction in the frequency of severe exacerbations of COPD. This strategy was associated with no overall increase in corticosteroid treatment; there was evidence that increased corticosteroid therapy was targeted to patients with eosinophilic airway inflammation and benefit was largely confined to these patients. I have shown an association
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Kölbeck, Karl-Gustav. "Nasal and bronchial airway reactivity in allergic and non allergic airway inflammation /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-428-3/.

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Wang, Jiahua. "The role of airway epithelium in airway inflammation and effect of corticosteroids." Thesis, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300175.

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Kelly, M. G. "Air way inflammation in obstructive airway diseases." Thesis, Queen's University Belfast, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273059.

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Ratnawati, Ratnawati Prince of Wale Hospital Clinical School UNSW. "Exhaled nitric oxide in asthmatic airway inflammation." Awarded by:University of New South Wales. Prince of Wale Hospital Clinical School, 2006. http://handle.unsw.edu.au/1959.4/25729.

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Measuring the level of exhaled NO (eNO) in the breath is a new method to monitor airway inflammation in asthma and may have a role in the management of asthma. The hypotheses were that eNO will reflect the degree of inflammation in chronic asthma, and will indicate how anti- inflammatory therapy should be altered to improve asthma control. Three studies were performed to test the hypotheses. A cross sectional study was performed to define the normal range of eNO and to compare this range with those who have asthma or atopy. The second study was observational, to compare the level of eNO during
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Gauvreau, Gail M. "Pharmacological modulation of allergen-induced airway inflammation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0001/NQ42847.pdf.

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Jatakanon, Anon. "Noninvasive assessment of airway inflammation in asthma." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312719.

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Books on the topic "Airway inflammation"

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Rogers, Duncan F., and Louise E. Donnelly. Human Airway Inflammation. Humana Press, 2001. http://dx.doi.org/10.1385/1592591515.

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Tony, Eissa N., and Huston David P, eds. Therapeutic targets in airway inflammation. Marcel Dekker, 2003.

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1947-, Nijkamp Franciscus Petrus, ed. Mediators in airway hyperreactivity. Birkhäuser Verlag, 1990.

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1940-, Olivieri D., and Bianco S, eds. Airway obstruction and inflammation: Present status and perspectives. Karger, 1990.

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Just, Allan. Exposure to Phthalate Mixtures and Inner-City Pediatric Allergic Disease and Airway Inflammation. [publisher not identified], 2012.

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Rosa, Maria Jose. Ambient combustion by-product exposures and exhaled biomarkers of airway inflammation and oxidative stress. [publisher not identified], 2014.

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Underwood, Stephen L. Studies on the mechanisms of pulmonary inflammation and airway hyperreactivity in animal models of asthma. University of East London, 1997.

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Gosman, Margot Madeleine Elvira. From pathology to treatment in chronic obstructive pulmonary disease: Focus on inflammatory cells and airway hyperresponsiveness. [s.n.], 2006.

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Wong, Simon S. Role of neprilysin in airway inflammation induced by diesel exhaust emissions: With a critique by the HEI Health Review Committee. Health Effects Institute, 2011.

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Page, Clive P., Katharine H. Banner, and Domenico Spina, eds. Cellular Mechanisms in Airways Inflammation. Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8476-1.

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Book chapters on the topic "Airway inflammation"

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Böning, Dieter, Michael I. Lindinger, Damian M. Bailey, et al. "Airway Inflammation." In Encyclopedia of Exercise Medicine in Health and Disease. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_4043.

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Rayees, Sheikh, and Inshah Din. "Airway Inflammation and Airway Hyperresponsiveness." In SpringerBriefs in Immunology. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-70270-0_3.

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Serbes, Mahir, Renato Cutrera, and Derya Altıntaş. "Airway Inflammation: United Airway in Children." In Comprehensive ENT. Springer Nature Switzerland, 2024. https://doi.org/10.1007/978-3-031-74853-0_33.

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Tesch, Jacob, Sumali Pandey, Radhika Adhikari, and Venkatachalem Sathish. "Inflammatory Mediators in the Airway: A Structural Cells’ Perspective." In Inflammation. Springer Nature Switzerland, 2025. https://doi.org/10.1007/978-3-031-55254-0_10-1.

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Kunkel, G., K. Nieber, K. Graf, J. Niehus, and C. R. Baumgarten. "Neuropeptides and Airway-Inflammation." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_61.

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Devalia, Jagdish Laxman, Jia Hua Wang, and Robert James Davies. "Airway epithelial cells." In Cellular Mechanisms in Airways Inflammation. Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8476-1_9.

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Wills-Karp, Marsha A., Andrea Keane-Myers, Stephen H. Gavett, and Douglas Kuperman. "Allergen-induced airway inflammation and airway hyperreactivity in mice." In In Vivo Models of Inflammation. Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-7775-6_6.

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Stewart, Alastair G., Darren J. Fernandes, Valentina Koutsoubos, et al. "Airway smooth muscle cells." In Cellular Mechanisms in Airways Inflammation. Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8476-1_10.

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Halayko, Andrew J., and Pawan Sharma. "Airway Smooth Muscle Cells." In Inflammation and Allergy Drug Design. Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444346688.ch12.

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Jeffery, Peter K. "Pathological spectrum of airway inflammation." In Cellular Mechanisms in Airways Inflammation. Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8476-1_1.

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Conference papers on the topic "Airway inflammation"

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Krumpe, Peter E. "Evolutionary Biology of Airway Clearance." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0372.

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Abstract The survival of air breathers depends upon maintaining clear airways. The primary defense of the airways under normal conditions is the mucociliary escalator. Only under conditions of airway inflammation does cough clearance mechanisms become predominant. In order to facilitate the expectoration of mucous and retained particulates, cells, and debris, coupling between the air stream and the mucous layer must occur. High linear velocity of the airstream and unstable flow regimes (vortices, eddies) facilitates development of waves in the mucous layer. Expectoration requires a catastrophi
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Pirogov, Aleksey, Anna Prikhodko, Evgeniya Afanas'eva, and Yuliy Perelman. "COMPARATIVE ASSESSMENT OF AIRWAY CELLULAR INFLAMMATION IN PATIENTS WITH BRONCHIAL ASTHMA IN RESPONSE TO HYPOSMOLAR AND COLD STIMULES." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9c45b256.10926397.

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An approach is presented to the study of cellular inflammation using cytological analysis of sputum in patients with bronchial asthma with different types of airway reaction to bronchoprovocation with cold air and distilled water. When the airways are hyperresponsive to hypoosmolar and cold stimuli, it has been established the activation of the neutrophilic component of bronchial granulocytes. Cold airway hyperresponsiveness is associated with an increase in neutrophil content and a concomitant decrease in the number of macrophages in the inflammatory pattern of the bronchi. An increase in spu
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Mattes, J., A. Collison, M. Plank, S. Phipps, and PS Foster. "MicroRNAs Regulate Allergic Airway Inflammation." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5456.

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Kim, HS, SK Ram, AT Ooi, et al. "Epigenetic Regulation ofFoxj1in Allergic Airway Inflammation." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2750.

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Short, Philip M., Samuel I. W. Lipworth, and Brian J. Lipworth. "Relationships Between Airway Hyper-Responsiveness, Airway Inflammation And Airway Calibre In Asthmatic Subjects." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4426.

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Harshman, T., M. L. Ford, B. W. Lewis, K. Heyob, and R. D. Britt. "JAK1 Inhibition Reduces Airway Inflammation and Increases Corticosteroid Sensitivity in a Severe Allergic Airway Inflammation Mouse Model." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a4455.

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Jackson-Humbles, DN, AM Audo, RF Buhs, NP Birmingham, JR Harkema, and JG Wagner. "Endotoxin Exacerbates Airway Inflammation but Attenuates Airway Hyperreactivity in Allergic Mice." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4257.

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Atabai, K., A. Kuo, A. Melton, et al. "Mfge8 Modulates the Severity of Allergic Airway Inflammation and Airway Hyperresponsiveness." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5455.

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Cohn, Lauren E., Karin Provost, Robert J. Homer, Naiqian Niu, and Charlotte Andreasen. "IFN-³ Acts On The Airway Epithelium To Regulate Allergic Airway Inflammation." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2485.

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Kumar, Nikila, Angela S. Benton, Jenifer Lerner, et al. "Airway Platelet Activation Is Associated With Airway Eosinophilic Inflammation In Asthma." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2805.

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Reports on the topic "Airway inflammation"

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Ma, He, Jifu Zhao, and Zhilei Wang. Efficacy and safety of HuaYu TongFu Method combined with acupuncture in the treatment of Acute Exacerbation of Chronic Obstructive Pulmonary Disease：A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.9.0114.

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Review question / Objective: This study is the protocol for a systematic review to evaluate the efficacy and safety of HuaYu TongFu Method combined with acupuncture in the treatment of Acute Exacerbation of Chronic Obstructive Pulmonary Disease. we conducted a systematic review and meta-analysis of published randomized clinical trials (RCTs) of such combined therapy in the treatment of AECOPD, It provides a reliable scientific basis for clinicians to use this approach to treat AECOPD. Condition being studied: Chronic obstructive pulmonary disease is the third leading cause of death worldwide.
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Czerwaty, Katarzyna, Karolina Dżaman, Krystyna Maria Sobczyk, and Katarzyna Irmina Sikrorska. The Overlap Syndrome of Obstructive Sleep Apnea and Chronic Obstructive Pulmonary Disease: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.11.0077.

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Review question / Objective: To provide the essential findings in the field of overlap syndrome of chronic obstructive pulmonary disease and obstructive sleep apnea, including prevalence, possible predictors, association with clinical outcomes, and severity compared to both chronic obstructive pulmonary disease and obstructive sleep apnea patients. Condition being studied: OSA is characterized by complete cessation (apnea) or significant decrease (hy-popnea) in airflow during sleep and recurrent episodes of upper airway collapse cause it during sleep leading to nocturnal oxyhemoglobin desatura
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Persisting Cryptococcus yeast species Vishniacozyma victoriae and Cryptococcus neoformans elicit unique airway inflammation in mice following repeated exposure (dataset). U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, 2023. http://dx.doi.org/10.26616/nioshrd-1061-2023-0.

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