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Relevant bibliographies by topics / Airway (Medicine) - Inflammation

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Academic literature on the topic 'Airway (Medicine) - Inflammation'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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

1

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

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

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

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

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

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

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

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

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

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

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

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

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Dissertations / Theses on the topic "Airway (Medicine) - Inflammation"

1

Fitch, Patrick Stephen. "A study of airway inflammation in childhood asthma." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326411.

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Ip, Sau-man Mary. "A pathophysiologic study of airway inflammation in bronchiectasis." [Hong Kong : University of Hong Kong], 1991. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13793895.

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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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葉秀文 and Sau-man Mary Ip. "A pathophysiologic study of airway inflammation in bronchiectasis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1991. http://hub.hku.hk/bib/B31981434.

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McKay, Anne. "The role of immune mediators in airway inflammation." Thesis, University of Glasgow, 2004. http://theses.gla.ac.uk/4828/.

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Asthma is a chronic inflammatory condition of the airways characterised by reversible airflow obstruction, airway hyper-responsiveness and inflammatory infiltrates in the airway walls containing eosinophils, T lymphocytes and mast cells. T helper (Th) lymphocyte subsets, defined by the cytokines they secrete, are thought to play a key role in the in the initiation and perpetuation of chronic airway inflammation. Th2 cells, producing interleukin (IL)-4, IL-5, IL-9 and IL-13, are thought to be of particular importance. In contrast, Thl cells producing interferon (IFN)-y may counteract the development of Th2 responses and so down-regulate the asthmatic response. The prevalence of asthma is increasing but the reasons for this are not fully understood. In addition, some patients do not respond adequately to treatment with corticosteroids, currently the most effective anti-inflammatory agents used routinely in human asthma. There is therefore continual interest in developing new therapeutic agents for asthma. A greater understanding of the regulation of inflammatory responses in asthma will assist in the identification of potential targets for therapeutic intervention. The aims of this thesis were (i) to assess the role of the cytokine IL-18 in allergic airway inflammation by determining IL-18 levels in induced sputum in asthmatic subjects in comparison to normal subjects, and by studies in a murine model of allergic asthma using IL-18 gene deficient mice and (ii) to assess the potential antiinflammatory actions of simvastatin and thymosin beta 4 sulfoxide in the murine asthma model. IL-18 is a pro-inflammatory cytokine which can promote IFN-y secretion and, in association with IL-12, enhance the development of Thl responses. However, in some circumstances it may also stimulate Th2 responses. IL-18 therefore has the potential to suppress or exacerbate allergic airway inflammation. The role of IL-18 in both clinical and experimental asthma remains unclear. Statins are inhibitors of the rate-limiting enzyme, 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, in cholesterol biosynthesis. As such they have been widely used as cholesterol lowering agents in clinical practice. They have previously been shown to have anti-inflammatory properties independent of their cholesterol-lowering ability in clinical studies of atherosclerotic disease and in animal models of Thlmediated inflammation. Thymosin beta 4 sulfoxide (T~4S0) is a 5 kDa peptide. Intracellularly its principal activity is to regulate actin polymerization. Corticosteroid treatment of monocytes in vitro induces the release of T~4S0 extracellularly, where it can inhibit neutrophil chemotaxis. Exogenous administration of T~4S0 has been shown to reduce neutrophilic inflammation in animal models. In this study it is shown that IL-18 is detectable in induced sputum fluid and IL-18 mRNA is expressed in induced sputum cells from asthmatic and nOlmal subjects. IL- 18 protein levels in induced sputum, and IL-18 mRNA expression in induced sputum cells were not significantly different between these groups. IL-18 production was localised to sputum macrophages. However, cigarette smoking significantly reduced IL-18 levels in induced sputum fluid in both asthmatic and normal subjects. In asthmatics, but not normal subjects, the reduction in IL-18 levels in sputum fluid was associated with reduced IL-18 mRNA expression in induced sputum cells. A murine model of allergic asthma, using BALB/C mice sensitised and challenged with ovalbumin (OVA), was used to examine the role of IL-18 in allergic responses in vivo. IL-18 gene knockout (ko) had significantly reduced bronchoalveolar lavage (BAL) total cell count and eosinophilia compared to wild-type (WT) mice. IL-18 ko mice had reduced IL-4 expression in thoracic lymph nodes, as assessed by quantitative peR, and significantly reduced OVA-specific IL-4 secretion from thoracic lymph node cultures assessed by ELISA. Serum OVA-specific IgG 1, IgG2a and IgE and total IgE levels were not significantly different between IL-18 ko and WT mice. The murine model of allergic asthma was also used to examine the anti-inflammatory activities of simvastatin and T~4S0 in a Th2-mediated, eosinophilic condition. Simvastatin treatment, either orally or intraperitoneally, and T~4S0 intraperitoneally reduced the total inflammatory cell infiltrate and eosinophilia in BAL fluid in response to inhaled OV A challenge. At higher doses of simvastatin intraperitoneally, a histological reduction in inflammatory infiltrates in the lungs was observed. Treatment with simvastatin intraperitoneally, but not orally, and T~4S0 were also associated with a reduction in IL-4 and IL-5 levels in BAL fluid. OVA-induced IL-4 and IL-5 secretion was reduced in thoracic lymph node cultures from both simvastatin-treated and T~4S0-treated mice. Neither simvastatin nor T~4S0 treatment altered serum total IgE or OVA-specific IgG 1 and IgG2a levels. The results described show that IL-18 can be detected in the induced sputum fluid of asthmatic and normal subjects and that cigarette smoking significantly reduces its levels. Studies in a murine model of allergic asthma suggest that IL-18 has a proinflammatory role in allergic airway inflammation, at least in part through its ability to induce IL-4 secretion. Both simvastatin and thymosin beta 4 sulfoxide had convincing anti-inflammatory properties in the murine model of asthma used, and these agents, or related compounds, may have therapeutic potential in human asthma.

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Laing, Ingrid A. "Candidate gene approach to investigating airway inflammation and asthma /." Connect to this title, 2004. http://theses.library.uwa.edu.au/adt-WU2005.0097.

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Zheng, Ling 1958. "Airway inflammation and remodelling post human lung transplantation." Monash University, Dept. of Medicine, 2002. http://arrow.monash.edu.au/hdl/1959.1/8099.

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Laing, Ingrid A. "Candidate gene approach to investigating airway inflammation and asthma." University of Western Australia. School of Paediatrics and Child Health, 2005. http://theses.library.uwa.edu.au/adt-WU2005.0097.

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[Truncated abstract] Asthma genetic studies have identified many genes that contribute to the pathogenesis of asthma and related variables. Members of the secretoglobin family appear to play an important role in controlling airway inflammation but they have received relatively little attention in asthma genetic research. In this thesis, I have investigated the genes of two members of the secretoglobin family (16 kDa Clara cell secretory protein (CC16) and secretoglobin 3A2 (SCGB3A2)) that are expressed at high levels in the airways and are important anti-inflammatory agents. The overall aim of these studies was to investigate the genetic variability of the CC16 and SCGB3A2 genes and their influence on airway inflammatory disease. The main hypothesis was that genetic variability in the genes for CC16 and SCGB3A2 exert an influence on airway inflammatory disease. Three populations were investigated: (1) a paediatric case control population (n=99), (2) an unselected birth cohort followed longitudinally at ages 1 month (n=244), six (n=123) and 11 years (n=195) and (3) an unselected Aboriginal Australian population (n=251). The case-control population was screened for novel DNA sequence variants in the CC16 promoter and the SCGB3A2 5’UTR and exons. No novel sequence variants were identified in the CC16 promoter and two were identified in the SCGB3A2 5’UTR (G- 811A and G-205A). A single nucleotide polymorphism previously identified in the CC16 gene (A38G) and the two polymorphisms identified in the SCGB3A2 gene were genotyped in both unselected populations. Genotype/phenotype associations were identified with adjustment for potential confounders such as age, gender, height and maternal tobacco smoking, where appropriate. This was due to the contribution of these factors to the aetiology of asthma, atopy and related phenotypes. All three polymorphism frequencies were significantly different between these two ethnically diverse populations

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Reader, Brenda Faye. "Social Stress Induces Immunoenhancement During Allergic Airway Inflammation and Infection." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1385475903.

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Stolarski, Bartosz. "The role of IL 33/ST2 pathway in innate immune response in airway inflammation." Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/2961/.

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Asthma is a common and complex inflammatory disease of the airways characterized by deregulated immune responses that involves activation of multiple cell types including Th2 cells, IgE producing B cells, mast cells, basophils and eosinophils as well as resident lung cells such as epithelial, smooth muscle cells and macrophages. Despite intensive research, there are still unmet needs in the treatment of asthma. Recently, a new cytokine of IL 1 family, named IL 33 emerged as a potentially important factor in the immunopathogenesis of allergy and asthma. It was recently shown in our laboratory that intranasal administration of IL 33 can induce certain physiological features that are characteristic of experimental asthma, such as eosinophilic inflammation, Th2 cytokine and antibody production as well as increased airway hyperresponsiveness. The effect of IL 33 on the activation and differentiation of allergen specific Th2 cells has been well studied. However, the contribution of IL 33 to the activation of lung resident and inflammatory innate cells remains undefined. In this project I focused on alveolar macrophages and eosinophils as both cell types were reported to express IL 33R, ST2L and are thought to play a crucial role in asthma pathogenesis. I raised the hypothesis that IL 33 released locally in the lungs may trigger symptoms resembling asthma through the activation of airway alveolar macrophages. Furthermore, I hypothesize that IL 33 may exacerbate and maintain inflammation in the lungs by the direct activation of eosinophils. In our previous study we showed that IL 33 could switch the quiescent phenotype of alveolar macrophages toward the alternatively activated phenotype (M2, AAM). In the first part of my thesis I looked at the consequences of this phenomenon for airway inflammation. Using clodronate liposomes in vivo I was able to eliminate macrophage population from the lungs and demonstrated that resident alveolar macrophages are crucial for the development of IL 33 induced eosinophilic inflammation in the airways. I then examined the contribution of IL 13, a known M2 differentiation factor, to airway inflammation. Using anti IL 13 neutralizing antibodies I showed that IL 13 is required for the IL 33 triggered differentiation of alveolar macrophages toward M2 phenotype as well as for eosinophilic inflammation. Next, I looked at how IL 33/ST2 pathway modulates the differentiation and activation of eosinophil. I demonstrated that bone marrow hematopoietic progenitors CD117+ express ST2L and that IL 33 is able to differentiate these cells toward eosinophils. By employing deficient mice or neutralizing antibodies I found that this process is ST2 and IL 5 dependent and independent of IL 13. I then extended my research interests to include mature mouse and human eosinophils. I showed that both human and mouse resting eosinophils express low levels of ST2L which can be markedly increased by IL 33. Moreover, I demonstrated that eosinophils that are recruited to the lungs during experimental allergic airway inflammation express high levels of ST2L. Furthermore, I carried out a study on effector function of eosinophils. I found that IL 33 induces IL 13, IL 6 and increases TARC, TGF production by mouse eosinophils. In addition, IL 33 exacerbated IgG induced human and mouse eosinophil degranulation, likely by enhancing FcRII expression. Having shown earlier that IL 13 is requited for the polarization of alveolar macrophages toward AAM by IL 33 in vitro and in light of the fact that IL 33 stimulated eosinophils can be a significant source of IL 13; I went on to investigate the interaction between macrophages and eosinophils. Using co cultures of ST2 / macrophages with WT eosinophils in Transwell system, I demonstrated that IL 33 but not IL 5 activated eosinophils can support macrophage polarization toward the pro inflammatory AAM phenotype, partially through the production of IL 13. Finally, given the role of IL 33/ST2L axis in eosinophil activation in vitro, I investigated the contribution of IL 33 activated eosinophils to airway inflammation in vivo. Using adoptive transfer protocol I showed that the contribution of IL 33 activated eosinophils to airway inflammation is mediated primarily by the release of cytokines from these cells which, in turn, recruits other inflammatory cells and supports the differentiation of alveolar macrophages towards AAM. These data show that IL 33/ST2 pathway regulates multiple features of alveolar macrophage and eosinophil biology that can have a significant impact on asthma pathophysiology in the airways. Studies carried out in our laboratory and elsewhere suggest that IL 33 is equally capable of activating other cell types that have been implicated in asthma pathology such as Th2, B1 cells, DCs, mast cells and basophils. Therefore, targeting IL 33/ST2 pathway may potentially offer a promising therapeutic approach to asthma and allergy.

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Books on the topic "Airway (Medicine) - Inflammation"

1

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

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2

(Editor), Clive P. Page, Katharine H. Banner (Editor), and Domenico Spina (Editor), eds. Cellular Mechanisms in Airways Inflammation (Progress in Inflammation Research). Birkhauser, 2000.

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(Editor), C. P. Page, Katharine H. Banner (Editor), and Domenico Spina (Editor), eds. Cellular Mechanisms in Airways Inflammation (Pir (Series).). Birkhauser, 2000.

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(Editor), Duncan F. Rogers, and Louise E. Donnelly (Editor), eds. Human Airway Inflammation: Sampling Techniques and Analytical Protocols (Methods in Molecular Medicine). Humana Press, 2001.

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(Editor), Johan Zaagsma, Herman Meurs (Editor), and Ad F. Roffel (Editor), eds. Muscarinic Receptors in Airways Diseases (Progress in Inflammation Research). Birkhauser, 2001.

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Book chapters on the topic "Airway (Medicine) - Inflammation"

1

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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Asghar Pasha, M., and Qi Yang. "Innate Lymphoid Cells in Airway Inflammation." In Advances in Experimental Medicine and Biology, 183–91. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63046-1_11.

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Wills-Karp, M., S. H. Gavett, Brian Schofield, and F. Finkelman. "Role of Interleukin-4 in the Development of Allergic Airway Inflammation and Airway Hyperresponsiveness." In Advances in Experimental Medicine and Biology, 343–47. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5855-2_48.

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Kowalski, Marek, Maria Sliwinska-Kowalska, James Baraniuk, and Michael Kaliner. "Morphology of Neurogenic Inflammation in the Airways: Plasma Protein Movement Across the Airway Mucosa and Epithelium." In Neuropeptides in Respiratory Medicine, 661–77. Taylor & Francis Group, 6000 Broken Sound Parkway NW, Suite 300, Boca Raton, FL 33487-2742: CRC Press, 2017. http://dx.doi.org/10.4324/9780203745915-32.

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Sutovska, M., M. Adamkov, M. Kocmalova, L. Mesarosova, M. Oravec, and S. Franova. "CRAC Ion Channels and Airway Defense Reflexes in Experimental Allergic Inflammation." In Advances in Experimental Medicine and Biology, 39–48. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4549-0_6.

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Kume, Hiroaki. "Role of Airway Smooth Muscle in Inflammation Related to Asthma and COPD." In Advances in Experimental Medicine and Biology, 139–72. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63046-1_9.

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Joskova, M., M. Sutovska, P. Durdik, D. Koniar, L. Hargas, P. Banovcin, M. Hrianka, V. Khazaei, L. Pappova, and S. Franova. "The Role of Ion Channels to Regulate Airway Ciliary Beat Frequency During Allergic Inflammation." In Advances in Experimental Medicine and Biology, 27–35. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/5584_2016_247.

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Hoffmeyer, F., V. van Kampen, A. Deckert, H. D. Neumann, M. Buxtrup, E. Willer, C. Felten, T. Brüning, M. Raulf, and J. Bünger. "Evaluation of Airway Inflammation in Compost Workers Exposed to Bioaerosols Using Exhaled Breath Condensate and Fractional Exhaled Nitric Oxide." In Advances in Experimental Medicine and Biology, 57–67. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/5584_2015_111.

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Emmett, Stevan R., Nicola Hill, and Federico Dajas-Bailador. "Respiratory Medicine." In Clinical Pharmacology for Prescribing. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780199694938.003.0011.

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Asthma is a reversible chronic airways condition characterized by airway obstruction, bronchial hyperresponsiveness and chronic inflammation. Exposure to triggers causes an inflammatory cascade and symptoms, such as wheeze, dyspnoea, and cough. It is the most common medical condition in children, affecting 1 in 10 to varying degree. Peaks in prevalence occur at 10 and 59 years of age, with a tendency towards those of an atopic (hypersensitive allergic/ genetic predisposition) nature. In asthma, there is a swing in balance between two opposing T- helper (Th) cell populations towards persistent and excessive T- helper cell type 2 (Th2) dominated immune responses. Th1 cells are involved in response to infection, while Th2 cells are responsible for cytokine production (e.g. IL- 4, IL- 5, IL- 6, IL- 9, and IL- 13) that are involved in allergic reaction, which may explain the overproduction of IgE, the presence of eosinophils and airway hyperresponsiveness. In the case of inhaled allergens, lung- based dendritic antigen- presenting cells ultimately stimulate Th2 cell production from naive Th0 cells (Figure 3.1). Aspirin and other NSAIDs can also initiate asthma symptoms, although this appears to be non- IgE dependant. Other dominant cells seen in asthma include mast cells and eosinophils. Mast cells, when activated by inhaled antigen, release bronchoconstrictive factors like histamine, cysteinyl-leukotrienes, prostaglandin D<sup>2</sup>, and eosinophil chemotactic factor. Mast cells in the airway may be sensitive to osmotic changes, thus account for exercise- induced asthma. The production of IL- 5 from activated Th2 and mast cells causes differentiation of eosinophils, which then migrate to the lung tissue, where they adhere to surface proteins like vascular- cell adhesion molecule 1 (VCAM- 1) and intercellular adhesion molecule 1 (ICAM- 1). Upon activation, these release pro- inflammatory cytokines like leukotrienes and granule proteins, which injure airway tissues. Additionally, eosinophil life is prolonged by the presence of IL- 4 and granulocyte- macrophage colony-stimulating factor (GM- CSF). Collectively, the persistence and presence of eosinophils may potentiate chronic inflammatory changes and this correlates closely with the clinical severity of disease. The overall cellular balance shift (Th2 dominance, mast cells, and eosinophils) and presence of an inflammatory stimulus results in bronchoconstriction (mainly via IgE- dependant release of mediators from mast cells constricting smooth muscle cells), airway oedema (through inflammation, mucus hypersecretion, and smooth muscle hypertrophy and hyperplasia), and airway hyperresponsiveness (through inflammation, dysfunctional neuroregulation, and structural changes).

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SK, Jindal. "Chapter-067 Airway Inflammation and Remodeling." In Textbook Of Pulmonary And Critical Care Medicine Vols 1 &amp 2, 866–75. Jaypee Brothers Medical Publishers (P) Ltd., 2011. http://dx.doi.org/10.5005/jp/books/11195_68.

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Conference papers on the topic "Airway (Medicine) - Inflammation"

1

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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Pirogov, Aleksey, Irina Andrievskaya, Anna Prikhodko, Viktor Kolosov, and Yuliy Perelman. "PHOSPHATASE ACTIVITY AND POSSIBILITIES OF LYSOSOMAL SECRETION OF AIRWAY NEUTROPHILS IN PATIENTS WITH BRONCHIAL ASTHMA IN COLD-INDUCED STRESS." 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_5fe01d9c3830b9.60748217.

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An approach to the study of cellular inflammation using methods of cytochemical analysis of sputum in patients with bronchial asthma with different types of airway reactions to bronchoprovocation with cold air is presented. Endotyping of patients contributes to a better understanding of the pathophysiological mechanisms and the choice of treatment tactics for the disease.

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Sutanto, Yusup Subagio, Levana Kasumadewi, Ana Rima Setijadi, and Hendra Kurniawan. "Effect of Thymoquinone on Interleukin-8, FEV1, and COPD Assessment Test Score in Stable Chronic Obstructive Lung Disease." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.05.34.

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ABSTRACT Background: Chronic obstructive pulmonary disease (COPD), a persistent airway obstruction, is caused by continuous exposure to harmful particles or irritants. Airway inflammation contributes the pathogenesis of COPD. Thymoquinone, has an anti-inflammatory effect. This study aimed to examine the effect of thymoquinone on interleukin-8 (IL-8) level, percentage of FEV1, and COPD assessment test score (CAT) in stable chronic obstructive lung disease. Subjects and Method: A quasi-experiment with pretest and posttest control group was conducted at the outpatient pulmonology unit, Dr. Moewardi, Surakarta, Central Java, from June to August 2019. A sample of 40 patients diagnosed with stable COPD was selected and allocated into two groups: (1) 20 patients treated with a combination of standard therapy and thymoquinone oil capsules 500 mg/ day; and (2) 20 patients treated with standard therapy. The dependent variables were IL-8 level, FEV1, and COPD assessment test score (CAT). The independent variables were treatment status. The data were analyzed by the paired-t-test. Results: The level of IL-8 was lower after treatment with combination of standard therapy and thymoquinone oil capsules 500 mg/ day (Mean= 14.35; SD= 3.95) than before treatment (Mean= 19.62; SD= 12.14), and it was not statistically significant (p= 0.052). The percentage of FEV1 was lower after treatment with combination of standard therapy and thymoquinone oil capsules 500 mg/ day (Mean= 42.36; SD= 14.43) than before treatment (Mean= 42.56; SD= 16.09), and it was not statistically significant (p= 0.943). The CAT score was lower after treatment with combination of standard therapy and thymoquinone oil capsules 500 mg/ day (Mean= 13.70; SD= 4.24) than before treatment (Mean= 13.70; SD= 4.24) than before treatment (Mean= 18.65; SD= 5.92), and it was statistically significant. Conclusion: Chronic obstructive pulmonary disease assessment test (CAT) score significantly decreases with the treatment combination of standard COPD therapy and thymoquinone oil capsules 500 mg/ day. Keywords: Thymoquinone, stable COPD, IL-8, FEV1, CAT score Correspondence: Yusup Subagio Sutanto. Department of Pulmonology and Respiratory Medicine, Dr. Moewardi Hospital Surakarta. Jl. Kolonel Soetarto No. 132 Surakarta, Central Java. Email: dr_yusupsubagio@yahoo.com. Mobile: +62811284165. DOI: https://doi.org/10.26911/the7thicph.05.34

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