Relevant bibliographies by topics / Airway inflammation

Academic literature on the topic 'Airway inflammation'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Airway inflammation"

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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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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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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, treatment with inhaled corticoteroids - the most effective treatment for asthma - improves symptoms and reduces the numbers of eosinophil s, mast cells and lymphocytes in the airways. The precise functions of the cells in promoting inflammation and causing asthma symptoms has not yet been fully elucidated. However, it is very likely that eicosanoids, such as the cysteinyl leukotrienes, are produced by eosinophils and mast cells and are a major cause of bronchoconstriction in asthma. Also, these inflammatory cells can produce proinflammatory cytokines, such as granulocytc-macrophage colony-stimulating factor. interleukin (IL) 3 and IL-5, which may promote continuing inflammation in the airways. Lastly, the persisting inflammatory cell infiltrate and products re leased from these cells arc very likely the cause or the airway structural changes characteristic of asthma, such as epithelial damage, goblet cell hyperplasia. smooth muscle thickening and deposition of collagen below the basement membrane. These changes have been suggested tn he the cause of airway hyperresponsiveness in asthma. An improved understanding of the precise mechanisms by which airway inflammation is initiated, propagates and causes airway damage will hopefully allow more precise treatment strategies to he developed for asthma than currently exist.
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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 and structural changes in asthma, and discusses how these processes may interact to modify airway function and induce respiratory symptoms.
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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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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 (April 1, 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 lead to acidification, including direct effects on epithelial cells or through recruitment of inflammatory cells. We demonstrated a partial role for eosinophils in airway acidification as CCR3 and IL-5-deficient mice had decreased extent of airway acidification in allergen-challenged mice. Furthermore, using dimethyl amiloride, a specific inhibitor of the Na+/H+ exchanger, we demonstrated significant inhibition of airway acidification in allergic airway inflammation, suggesting a role for ion (proton) channels. In summary, our studies demonstrate that mouse airways are acidified during allergic airway inflammation. We also showed that the mechanism of airway acidification in asthma involves IL-13-mediated pathways including eosinophils and proton channels. These results have considerable implications for the development of therapies that target airway acidification.
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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 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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Takahashi, Kentaro, Koichi Hirose, Saki Kawashima, Yusuke Niwa, Hidefumi Wakashin, Arifumi Iwata, Koji Tokoyoda, Toshinori Nakayama, and Hiroshi Nakajima. "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 (May 1, 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 lung epithelial cell line (MLE-15 cells). RESULTS: Antigen inhalation induced IL-22 production in CD4(+) T cells. Only one third of IL-22-producing CD4(+) T cells also produced IL-17A. Anti-IL-22 antibody administration enhanced antigen-induced IL-13 production, eosinophil recruitment, and goblet cell hyperplasia in the airways. On the other hand, intranasal administration of rIL-22 attenuated eosinophil recruitment. Moreover, anti-IL-22 antibody enhanced IL-25 production in the airways, and anti-IL-25 antibody reversed the enhancing effect of anti-IL-22 antibody on eosinophil recruitment into the airways. Finally, IL-22 inhibited IL-13-mediated enhancement of IL-25 expression in IL-1β- or LPS-stimulated MLE-15 cells. CONCLUSION: IL-22 attenuates antigen-induced airway inflammation, possibly by inhibiting IL-25 production by lung epithelial cells.
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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 (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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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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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 may also decrease FENO indirectly by converting airway NO to NOx. It was found that EBC volume was significantly correlated with both tidal volume and minute volume. Comparing four EBC collection devices demonstrated greater efficiency with the ECoScreen?? than siliconised glass tubes or RTube?? but it gave factitiously high NOx levels. Total EBC protein levels over a 10-minute collection were significantly higher using the ECoScreen?? than either glass or RTube?? devices. A cross-sectional study of 96 COPD patients and 80 age-matched control subjects demonstrated that FENO levels in COPD patients were significantly higher than normal subjects when comparing either the combined groups or appropriate two subgroups: ex-smokers and smokers. GCS treatment demonstrated no significant effect on either FENO levels or EBC NOx, but EBC NOx was elevated in smokers. In vitro, cigarette smoke extract (CSE) induced significantly higher NOx and asymmetric dimethylarginine (ADMA) levels in A549 cells when compared with control media. The anti-oxidant, NAC pre-treatment partially reversed the elevated NOx levels but not the ADMA levels. This thesis is the first to report FENO and EBC NOx in COPD patients in an appropriate sample size to be able to evaluate each subgroup, and the increased EBC NOx levels found in smokers in vivo was consistent with the elevated NOx level in response to CSE observed in vitro. These data indicate that smoking-related airway inflammation and activation of the NO pathway are complex with both an increase in ADMA, NO, NOx and may be regulated by oxidative stress rather than the nitric oxide synthase (NOS) pathway.
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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 between the sputum differential neutrophil count and airway bacterial load, and showed that a one week course of Levofloxacin significantly reduced both the % neutrophil count and bacterial load in patients with stable state COPD and bacterial load > 106 cfu/ml. I have shown that the prevalence of peptic ulcer disease increases progressively with increasing severity of COPD in miners with homogeneous risk factors for development of COPD, and that peptic ulceration was a strong and independent predictor of a low FEV1 % predicted and FEV1/FVC ratio. In another population I showed that H.Pylori seropositivity was more common in patients with COPD compared to healthy smokers matched for age and occupation.;We have shown that TREM-1 can be measured from induced sputum and is potentially a novel marker of bacterial infection and neutrophilic airway inflammation during exacerbations.;Further work is required to ensure that measurement and modulation of airway inflammation results in improved clinical outcomes, and is made more clinically viable.
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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 and after an exacerbation of asthma. The third study was an interventional study to evaluate eNO in management of paediatric asthma. In this latter study the level of eNO was measured to monitor airway inflammation in asthmatic children with the intention of adjusting antiinflammatory drugs (inhaled glucocorticosteroids) according to the level of eNO. These studies have shown that the mean level of eNO was significantly higher in asthmatic compared with normal subjects, but not significantly different when compared with atopic non-asthmatic subjects. eNO was correlated with the number of positive skin prick tests in atopic subjects whether asthmatic or nonasthmatic. The eNO level was increased during acute exacerbations of asthma and decreased after two weeks with therapy of GCS. In a pilot study eNO appeared to be superior to FEV1 in adjusting the dose of iGCS to control asthmatic children, but this needs to be confirmed with a larger sample size. Another non-invasive method to detect inflammatory markers is the technique of exhaled breath condensate (EBC). Although NO is degraded to NOx, it was found that eNO had no significant correlation with EBC NOx but had a significant correlation with pH. Hypertonic saline challenge, an artificial model of an asthmatic exacerbation was associated with an increase in EBC volume and the release of histamine, implicating mast cell activation. These novel findings suggest that non-invasive markers can be used both for clinical and mechanistic proposes.
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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. New Jersey: 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. New York: Marcel Dekker, 2003.

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

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

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

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Eissa, N. Tony, and David P. Huston. Therapeutic Targets in Airway Inflammation. Taylor & Francis Group, 2003.

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Eissa, N. Tony, and David P. Huston. Therapeutic Targets in Airway Inflammation. Taylor & Francis Group, 2003.

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Eissa, N. Tony, and David P. Huston, eds. Therapeutic Targets in Airway Inflammation. CRC Press, 2003. http://dx.doi.org/10.3109/9780203911471.

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Eissa, N. Tony, and David P. Huston. Therapeutic Targets in Airway Inflammation. Taylor & Francis Group, 2003.

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Eissa, N. Tony, and David P. Huston. Therapeutic Targets in Airway Inflammation. Taylor & Francis Group, 2003.

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Book chapters on the topic "Airway inflammation"

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Böning, Dieter, Michael I. Lindinger, Damian M. Bailey, Istvan Berczi, Kameljit Kalsi, José González-Alonso, David J. Dyck, et al. "Airway Inflammation." In Encyclopedia of Exercise Medicine in Health and Disease, 52. Berlin, Heidelberg: 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, 7. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-70270-0_3.

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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, 307–11. Boston, MA: 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, 245–62. Basel: 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, 137–58. Basel: 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, Aurora Messina, Claire E. Ravenhall, Ross Vlahos, and Kai-Feng Xu. "Airway smooth muscle cells." In Cellular Mechanisms in Airways Inflammation, 263–302. Basel: 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, 163–71. Oxford, UK: 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, 1–52. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8476-1_1.

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Goyal, Vikas, and Anne B. Chang. "Acute Exacerbations of Airway Inflammation." In Compendium of Inflammatory Diseases, 5–20. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_196.

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Koeppen, Michael, Francesco Di Virgilio, Eric T. Clambey, and Holger K. Eltzschig. "Purinergic Regulation of Airway Inflammation." In Purinergic Regulation of Respiratory Diseases, 159–93. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1217-1_7.

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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 catastrophic separation of mucous from underlying airway structures. The response of airways is initially to secrete a deeper mucous layer, and to remodel airway glands to produce a mucous blend having a higher elastic modulus. Mucous rheologic properties seem to be tailored by the presence of inflammation to become more easily cleared, even at lower air flow rates which are characteristic of lung disease. Airway oscillations (wheezes and rhonchi) which are physical findings associated with airway inflammation may further enhance mucous clearance by adding additional energy to the mucous layer, aiding catastrophic separation. Thus airway clearance is a highly evolved and coordinated example of evolutionary biology.
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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 sputum cytosis is inherent in a positive airway response to a hypoosmolar test with an unexpressed dynamics of the level of bronchial eosinophils.
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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, DW Nickerson, JA Belperio, TA Chatila, and BN Gomperts. "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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Pidaparti, Ramana M., and Kevin R. Ward. "Airway Inflammation Induced by Mechanical Ventilation Through Multiscale Modeling." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80174.

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Inflammation has been recognized as a major integral component for most of the acute and chronic diseases. Inflammation can be initiated within the body as an innate process or by external factors such as infections and trauma. Inflammation is a complex and dynamic process, and involves nonlinearity and stochasticity. Without the inflammation, the harmful stimuli cannot be removed and the healing process cannot occur. However, an over-expression or under-expression of inflammatory responses can lead to severe consequences, such as Multiple Organ Dysfunction Syndrome (MODS), which is characterized by sequential organ failure. Acute lung injury (ALI) is typically one of the first manifestation of MODS. It can be triggered by external stimuli such as pathogens or from inflammatory mediators produced from various other processes ranging from other damaged organs or to blood transfusions to even the biomechanical forces of mechanical ventilation itself.
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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, N. Azhar, M. Lam, S. Jame, and D. Sheppard. "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, Andrew Wiles, Matthew Foerster, Stephen J. Teach, and Robert J. Freishtat. "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, September 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. AECOPD is the most common cause of hospitalization and death in patients with COPD. As lung function deteriorates and the disease progresses, the risk of alveolar hypoxia and consequent hypoxemia increases. Inflammation plays an important role in the progression of AECOPD. Modern medicine mainly treats AECPD by anti-inflammatory, relief of airway spasm, glucocorticoids, inhalants and other methods. Long-term application can easily lead to bacterial flora imbalance and drug resistance in patients. Comparatively, traditional Chinese medicine and acupuncture therapy are safe and effective.To assess the therapeutic efficacy and safety of HuaYu TongFu Method combined with acupuncture in AECOPD, we created a protocol for a systematic review to inform future clinical applications.
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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, November 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 desaturations and arousals from rest. The recurrent arousals which occur in OSA lead to neurocognitive consequences, daytime sleepiness, and reduced quality of life. Because of apneas and hypopneas, patients are experiencing hypoxemia and hypercapnia, which result in increasing levels of catecholamine, oxidative stress, and low-grade inflammation that lead to the appearance of cardio-metabolic consequences of OSA. COPD is a chronic inflammatory lung disease defined by persistent, usually pro-gressive AFL (airflow limitation). Changes in lung mechanics lead to the main clini-cal manifestations of dyspnea, cough, and chronic expectoration. Furthermore, patients with COPD often suffer from anxiety and depression also, the risk of OSA and insomnia is higher than those hospitalized for other reasons. Although COPD is twice as rare as asthma but is the cause of death eight times more often.
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