Relevant bibliographies by topics / Airway eosinophilia

Academic literature on the topic 'Airway eosinophilia'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Airway eosinophilia"

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Johansson, Kristina Britt Charlotte, Carina Malmhäll, Patricia Ramos-Ramírez, and Madeleine Rådinger. "IL-33 elicits IL-5 dependent eosinophilia in vivo." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 194.8. http://dx.doi.org/10.4049/jimmunol.198.supp.194.8.

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Abstract Introduction Interleukin (IL)-33 plays important roles in the immunopathogenesis of allergy and asthma. It acts by promoting IL-5 and IL-13 secretion from IL-33 responsive type 2 innate lymphoid cells (ILC2s) or directly activates eosinophils and mast cells. IL-5 is crucial in eosinophilic inflammation by controlling differentiation and survival of eosinophils in the bone marrow as well as release and recruitment of eosinophils to the airways. While ILC2s have emerged as important producers of IL-5 in airways, the cellular source of IL-5 in the bone marrow is less explored. In this study we tested the hypothesis that IL-33 induced airway eosinophilia is an IL-5 dependent process in which ILC2s produce IL-5 locally in the bone marrow. Methods IL-5 production by bone marrow ILC2s was analyzed by intracellular flow cytometry in a murine model of IL-33 induced airway eosinophilia. Results Intranasal IL-33 administration resulted in eosinophil infiltration in airways and increased eosinophils in bone marrow. It was accompanied by a dramatic induction of eotaxin-2 in airways, indicating eosinophil recruitment to the tissue. IL-5+ ILC2s as well as expression of the IL-33 receptor on ILC2s increased in the bone marrow in response to IL-33 administration. Importantly, airway and bone marrow eosinophils were greatly reduced in mice pre-treated with anti-IL-5 antibodies followed by intranasal IL-33. Conclusion Our results demonstrate that IL-33 elicits IL-5 dependent eosinophilia in vivo, where ILC2s represent a local source of IL-5 in the bone marrow.
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Cusack, Ruth P., Christiane E. Whetstone, Yanqing Xie, Maral Ranjbar, and Gail M. Gauvreau. "Regulation of Eosinophilia in Asthma—New Therapeutic Approaches for Asthma Treatment." Cells 10, no. 4 (April 6, 2021): 817. http://dx.doi.org/10.3390/cells10040817.

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Asthma is a complex and chronic inflammatory disease of the airways, characterized by variable and recurring symptoms, reversible airflow obstruction, bronchospasm, and airway eosinophilia. As the pathophysiology of asthma is becoming clearer, the identification of new valuable drug targets is emerging. IL-5 is one of these such targets because it is the major cytokine supporting eosinophilia and is responsible for terminal differentiation of human eosinophils, regulating eosinophil proliferation, differentiation, maturation, migration, and prevention of cellular apoptosis. Blockade of the IL-5 pathway has been shown to be efficacious for the treatment of eosinophilic asthma. However, several other inflammatory pathways have been shown to support eosinophilia, including IL-13, the alarmin cytokines TSLP and IL-33, and the IL-3/5/GM-CSF axis. These and other alternate pathways leading to airway eosinophilia will be described, and the efficacy of therapeutics that have been developed to block these pathways will be evaluated.
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Oliver, Brian, Katrina Tonga, David Darley, Sandra Rutting, Xin Zhang, Hui Chen, and Gang Wang. "COPD treatment choices based on blood eosinophils: are we there yet?" Breathe 15, no. 4 (December 2019): 318–23. http://dx.doi.org/10.1183/20734735.0254-2019.

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Eosinophils are increasingly being recognised as an important characteristic feature of COPD. Patients with COPD and eosinophilic inflammation tend to respond to steroid therapy; however, many questions remain regarding the optimum measurement. Eosinophilic inflammation may be defined based on various sampling techniques, including eosinophil levels in blood, sputum, bronchoalveolar lavage or biopsy, which leads to inconsistencies in its definition. Blood eosinophils may increase in conjunction with sputum eosinophils during COPD exacerbations and therefore may be a good surrogate marker of airway eosinophilic inflammation. However, the timing of the blood eosinophil measurement, the stability of the eosinophil count and the threshold used in different studies are variable. The use of blood eosinophil count to direct biological therapies in COPD has also had variable outcomes. Eosinophilic inflammation has an important role in COPD management; however, its use as the optimum biomarker still needs further investigation.Key pointsEosinophilia may play a significant role in the pathogenesis of COPD.Eosinophilic inflammation in COPD can be steroid responsive; however, eosinophilic inflammation is variable, and caution needs to be taken with measurements and the thresholds used.The long-term effects of reducing eosinophil levels in COPD is unclear.Educational aimsTo explore current knowledge of eosinophils in COPD.To explore the relationship between eosinophilia and corticosteroid use.To understand the limitations of assessing and using eosinophilia in COPD.
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Broide, David, Jurgan Schwarze, Helen Tighe, Tim Gifford, Minh-Duc Nguyen, Siamak Malek, John Van Uden, Elena Martin-Orozco, Erwin W. Gelfand, and Eyal Raz. "Immunostimulatory DNA Sequences Inhibit IL-5, Eosinophilic Inflammation, and Airway Hyperresponsiveness in Mice." Journal of Immunology 161, no. 12 (December 15, 1998): 7054–62. http://dx.doi.org/10.4049/jimmunol.161.12.7054.

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Abstract We have used a mouse model of allergen-induced airway hyperresponsiveness to demonstrate that immunostimulatory DNA sequences (ISS) containing a CpG DNA motif significantly inhibit airway eosinophilia and reduce responsiveness to inhaled methacholine. ISS not only inhibited eosinophilia of the airway (by 93%) and lung parenchyma (91%), but also significantly inhibited blood eosinophilia (86%), suggesting that ISS was exerting a significant effect on the bone marrow production of eosinophils. The inhibition of the bone marrow production of eosinophils by 58% was associated with a significant inhibition of T cell-derived cytokine generation (IL-5, granulocyte-macrophage CSF, and IL-3). ISS exerted this inhibitory effect on T cell cytokine production indirectly by stimulating monocytes/macrophages and NK cells to generate IL-12 and IFNs. The onset of the ISS effect on reducing the number of tissue eosinophils was both immediate (within 1 day of administration) and sustained (lasted 6 days), and was not due to ISS directly inducing eosinophil apoptosis. ISS was effective in inhibiting eosinophilic airway inflammation when administered either systemically (i.p.), or mucosally (i.e., intranasally or intratracheally). Interestingly, a single dose of ISS inhibited airway eosinophilia as effectively as daily injections of corticosteroids for 7 days. Moreover, while both ISS and corticosteroids inhibited IL-5 generation, only ISS was able to induce allergen-specific IFN-γ production and redirect the immune system toward a Th1 response. Thus, systemic or mucosal administration of ISS before allergen exposure could provide a novel form of active immunotherapy in allergic diseases.
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Salter, Brittany M., Xiaotian Ju, and Roma Sehmi. "Eosinophil Lineage-Committed Progenitors as a Therapeutic Target for Asthma." Cells 10, no. 2 (February 16, 2021): 412. http://dx.doi.org/10.3390/cells10020412.

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Eosinophilic asthma is the most prevalent phenotype of asthma. Although most asthmatics are adequately controlled by corticosteroid therapy, a subset (5–10%) remain uncontrolled with significant therapy-related side effects. This indicates the need for a consideration of alternative treatment strategies that target airway eosinophilia with corticosteroid-sparing benefits. A growing body of evidence shows that a balance between systemic differentiation and local tissue eosinophilopoietic processes driven by traffic and lung homing of bone marrow-derived hemopoietic progenitor cells (HPCs) are important components for the development of airway eosinophilia in asthma. Interleukin (IL)-5 is considered a critical and selective driver of terminal differentiation of eosinophils. Studies targeting IL-5 or IL-5R show that although mature and immature eosinophils are decreased within the airways, there is incomplete ablation, particularly within the bronchial tissue. Eotaxin is a chemoattractant for mature eosinophils and eosinophil-lineage committed progenitor cells (EoP), yet anti-CCR3 studies did not yield meaningful clinical outcomes. Recent studies highlight the role of epithelial cell-derived alarmin cytokines, IL-33 and TSLP, (Thymic stromal lymphopoietin) in progenitor cell traffic and local differentiative processes. This review provides an overview of the role of EoP in asthma and discusses findings from clinical trials with various therapeutic targets. We will show that targeting single mediators downstream of the inflammatory cascade may not fully attenuate tissue eosinophilia due to the multiplicity of factors that can promote tissue eosinophilia. Blocking lung homing and local eosinophilopoiesis through mediators upstream of this cascade may yield greater improvement in clinical outcomes.
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Vucevic, Danijela, Tatjana Radosavljevic, and Gordana Djordjevic-Denic. "The role of eosinophilic leukocytes in pathogenesis of bronchial asthma." Jugoslovenska medicinska biohemija 23, no. 4 (2004): 333–41. http://dx.doi.org/10.2298/jmh0404333v.

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Pathogenesis of bronchial asthma has not been completely understood. Eosinophilic leukocytes accumulate in high numbers in the lungs, blood and sputum of asthmatic patients. Peripheral blood eosinophilia has been identified as a risk factor for the development of airway obstruction. Prominent eosinophilic inflammatory infiltrate in the bronchial mucosa and correlation between eosinophil numbers and disease severity supports the hypothesis that eosinophils are central inflammatory cells capable of inducing pathophysiological features of asthma. Activated eosinophils secrete a wide range of preformed and newly generated mediators that damage the bronchial epithelium, contract smooth muscle, increase mucous secretion and cause vasodilatation. There is ample evidence that oxidants generation is increased during an asthma exacerbation. Many investigations indicate that airway and blood eosinophils produce more oxidants in asthmatic patients compared with control subjects.
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Drake, Matthew G., Gregory D. Scott, Emily D. Blum, Katherine M. Lebold, Zhenying Nie, James J. Lee, Allison D. Fryer, Richard W. Costello, and David B. Jacoby. "Eosinophils increase airway sensory nerve density in mice and in human asthma." Science Translational Medicine 10, no. 457 (September 5, 2018): eaar8477. http://dx.doi.org/10.1126/scitranslmed.aar8477.

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In asthma, airway nerve dysfunction leads to excessive bronchoconstriction and cough. It is well established that eosinophils alter nerve function and that airway eosinophilia is present in 50 to 60% of asthmatics. However, the effects of eosinophils on airway nerve structure have not been established. We tested whether eosinophils alter airway nerve structure and measured the physiological consequences of those changes. Our results in humans with and without eosinophilic asthma showed that airway innervation and substance P expression were increased in moderate persistent asthmatics compared to mild intermittent asthmatics and healthy subjects. Increased innervation was associated with a lack of bronchodilator responsiveness and increased irritant sensitivity. In a mouse model of eosinophilic airway inflammation, the increase in nerve density and airway hyperresponsiveness were mediated by eosinophils. Our results implicate airway nerve remodeling as a key mechanism for increased irritant sensitivity and exaggerated airway responsiveness in eosinophilic asthma.
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Schwarze, Jürgen, Grzegorz Cieslewicz, Anthony Joetham, Toshihide Ikemura, Eckard Hamelmann, and Erwin W. Gelfand. "CD8 T Cells Are Essential in the Development of Respiratory Syncytial Virus-Induced Lung Eosinophilia and Airway Hyperresponsiveness." Journal of Immunology 162, no. 7 (April 1, 1999): 4207–11. http://dx.doi.org/10.4049/jimmunol.162.7.4207.

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Abstract Viral respiratory infections can cause bronchial hyperresponsiveness and exacerbate asthma. In mice, respiratory syncytial virus (RSV) infection results in airway hyperresponsiveness (AHR) and eosinophil influx into the airways. The immune cell requirements for these responses to RSV infection are not well defined. To delineate the role of CD8 T cells in the development of RSV-induced AHR and lung eosinophilia, we tested the ability of mice depleted of CD8 T cells to develop these symptoms of RSV infection. BALB/c mice were depleted of CD8 T cells using anti-CD8 Ab treatment before intranasal administration of infectious RSV. Six days postinfection, airway responsiveness to inhaled methacholine was assessed by barometric body plethysmography, and numbers of lung eosinophils and levels of IFN-γ, IL-4, and IL-5 in bronchoalveolar lavage fluid were monitored. RSV infection resulted in airway eosinophilia and AHR in control mice, but not in CD8-depleted animals. Further, whereas RSV-infected mice secreted increased amounts of IL-5 into the airways as compared with noninfected controls, no IL-5 was detectable in both bronchoalveolar lavage fluid and culture supernatants from CD8-depleted animals. Treatment of CD8-depleted mice with IL-5 fully restored both lung eosinophilia and AHR. We conclude that CD8 T cells are essential for the influx of eosinophils into the lung and the development of AHR in response to RSV infection.
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Rajavelu, Priya, Madhavi Rayapudi, Matthew Moffitt, Akanksha Mishra, and Anil Mishra. "Significance of para-esophageal lymph nodes in food or aeroallergen-induced iNKT cell-mediated experimental eosinophilic esophagitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 302, no. 7 (April 1, 2012): G645—G654. http://dx.doi.org/10.1152/ajpgi.00223.2011.

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Eosinophilic esophagitis (EoE) is a recently recognized inflammatory disorder driven by food hypersensitivity; however, the specific foods and mechanisms involved are unclear. In patients with EoE, we have found that hypersensitivities to corn and peanuts are the most common. Accordingly, we sensitized and exposed mice either intranasally or intragastrically with corn or peanut extract or saline. Esophageal eosinophilia, the genes of eosinophil-directed cytokines, and allergen-induced antibodies were examined in mice challenged with corn or peanut extract or saline. A high number of esophageal lamina propria eosinophils as well as eosinophilic microabscesses, intraepithelial eosinophils, extracellular eosinophilic granules, thickened and disrupted epithelial mucosa, and mast cell hyperplasia were observed in the esophagus of peanut or corn allergen-challenged mice. Mechanistic analysis indicated that para-esophageal lymph nodes might be critical in the trafficking of eosinophils to the esophagus and in EoE association to airway eosinophilia. Furthermore, experimentation with gene-targeted mice revealed that peanut allergen-induced EoE was dependent on eotaxin and invariant natural killer T (iNKT) cells, as CD1d and eotaxin-1/2 gene-deficient mice were protected from disease induction. Thus we provide evidence that para-esophageal lymph nodes are involved in food- or aeroallergen-induced eosinophilia and patchy EoE pathogenesis, likely a mechanism dependent on eotaxins and iNKT cells.
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Brussino, L., E. Heffler, C. Bucca, S. Nicola, and G. Rolla. "Eosinophils Target Therapy for Severe Asthma: Critical Points." BioMed Research International 2018 (October 25, 2018): 1–6. http://dx.doi.org/10.1155/2018/7582057.

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Asthma is a chronic and heterogeneous disease, which is defined as severe disease whenever it requires treatment with a high dose of inhaled corticosteroids plus a second controller and/or systemic corticosteroids to prevent it from becoming ‘‘uncontrolled’’ or if it remains ‘‘uncontrolled’’ despite this therapy. Severe asthma is a heterogeneous condition consisting of phenotypes such as eosinophilic asthma, which is characterized by sputum eosinophilia, associated with mild to moderate increase in blood eosinophil count, frequently adult-onset, and associated with chronic rhinosinusitis with nasal polyps in half of the cases. Eosinophilic asthma is driven by T2 inflammation, characterized, among the others, by interleukin-5 production. IL-5 plays a key role in the differentiation, survival, migration, and activation of eosinophils, and it has become an appealing therapeutic target for eosinophilic asthma. In recent years two monoclonal antibodies (mepolizumab and reslizumab) directed against IL-5 and one monoclonal antibody directed against the alpha-subunit of the IL-5 receptor (benralizumab) have been developed. All these IL-5 target drugs have been shown to reduce the number of exacerbation in patients with severe asthma selected on the basis of peripheral blood eosinophil count. There are still a number of unresolved issues related to the anti-IL5 strategy in eosinophilic asthma, which are here reviewed. These issues include the effects of such therapy on airway obstruction and asthmatic symptoms, the level of baseline eosinophils that predicts a response to treatment, the relationship between blood and airway eosinophilia, and, perhaps most importantly, how to elucidate the pathogenetic role played by eosinophils in the individual patient with severe eosinophilic asthma.
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Dissertations / Theses on the topic "Airway eosinophilia"

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Birrell, Mark Andrew. "Characterisation of animal models of airway eosinophilia." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408172.

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De, Campo Benjamin. "The influence of PAR activators on allergen-induced pulmonary eosinophilia and hyperresponsiveness in mice /." Connect to this title, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0060.

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Brightling, Christopher. "Airway eosinophilia in chronic cough, asthma and chronic obstructive pulmonary disease : an immunopathological feature of disease and a marker of response to corticosteriods." Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/29409.

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Eosinophilia bronchitis is a condition characterised by chronic cough and a sputum eosinophilia without the variable airflow obstruction or airway hyperresponsiveness characteristics of asthma. This thesis describes the incidence of eosinophilic bronchitis as a cause of chronic cough and determines whether the presence of a sputum eosinophilia is associated with a favourable response to corticosteroids in eosinophilic bronchitis and chronic obstructive pulmonary disease (COPD). This is the first study to investigate in detail the immunopathology of patients with eosinophilic bronchitis compared to asthma. Understanding differences in the immunopathology will inform our understanding of the development of the disordered airway physiology observed in asthma. We demonstrated that eosinophilic bronchitis is a common cause of chronic cough and that a sputum eosinophilia predicts a good response to corticosteroids in this condition, asthma and COPD. We found sputum, bronchial wash and bronchoalveolar lavage (BAL) eosinophilia and bronchial submucosal evidence of eosinophilic airway inflammation, increased Th2 cytokine expression and basement membrane thickening and increased constitutive intracellular expression of IL-4 from BAL derived T-cells in subjects with eosinophilic bronchitis to the same degree as those with asthma. Thus, the immunopathology of eosinophilic bronchitis is very similar to asthma questioning the importance of these classical pathological characteristic of asthma in the development of abnormal airway physiology. In addition, we quantified the inflammatory cell infiltration of the airway smooth muscle and found a striking increase in the number of mast cells within the airway smooth muscle in asthma compared to eosinophilic bronchitis and normal subjects. Our findings suggest that in asthma the microlocalisation of mast cells within the airway smooth muscle is a key factor in the development of variable airflow obstruction and airway hyperresponsiveness. Thus, specific targeting of the mast cell-smooth muscle interaction may provide a novel approach to the effective treatment for asthma.
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Kottyan, Leah Claire. "Airway Acidification in Asthma." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1280778640.

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Humbles, Alison Anita. "The relationship between the generation of an eosinophil-selective chemoattractant, ecotoxin and eosinophil accumulation in vivo." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267879.

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Eltboli, Osama M. I. "Eosinophilic airways inflammation in Chronic Obstructive Pulmonary Disease." Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/32546.

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Background: Eosinophilic airway inflammation (>3% sputum eosinophils) is a feature of subgroup of subjects with chronic obstructive pulmonary disease (COPD). My objectives were to investigate the clinical characteristics of eosinophilic COPD, its stability over time and extent in bronchial tissue, whether it is related to parasite exposure or atopy and whether its persistence is due to abnormal clearance by macrophages. Methods: Subjects were studied that had participated in previous observational studies. The repeatability of sputum eosinophils was measured between 3 monthly visits for 1 year. The extent of eosinophilic inflammation in bronchial tissue was assessed using immunohistology on bronchial tissue from COPD and control subjects. Positive serology for parasites was tested in serum samples for 4 helminth species. Atopy was assessed in the subjects using serum total Ig-E and skin prick test. Eosinophil efferocytosis by macrophages was investigated in vivo using cytoplasmic area of red hue of macrophages and in vitro using apoptotic eosinophils fed to monocyte-derived macrophages from COPD and healthy controls. The dynamics of eosinophil clearance during exacerbations was explored using the red hue technique. Results: Eosinophilic and non-eosinophilic COPD have similar lung function and exacerbation frequency. In eosinophilic COPD the health status is better and bacterial colonisation is lower. This phenotype is stable over time. Airway tissue eosinophilis are increased in COPD subjects with high blood eosinophils and are positively correlated with features of remodelling. Eosinophilic COPD is not associated with helminth exposure, but is related to elevated total Ig-E. Macrophage efferocytosis of eosinophils is impaired in COPD and is associated with the severity and frequency of COPD exacerbations. Efferocytosis of eosinophils by macrophages is increased following oral corticosteroid therapy at exacerbation. Conclusion: Eosinophilic COPD is a distinct and stable phenotype that persists in the blood, bronchus and sputum. Its persistence is partly related to atopy and impaired clearance by macrophages with the latter associated with COPD exacerbation severity and frequency.
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Hallsworth, Matthew Pearce. "GM-CSF and eosinophil survival in asthma." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341883.

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Fulkerson, Patricia C. "A Critical Role for Eosinophils and CCR3 Signal Transduction in Allergic Airway Disease." University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1120337075.

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Lavinskienė, Simona. "Peripheral blood neutrophil and eosinophil activity during allergen-induced late-phase airway inflammation in asthma." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2015. http://vddb.library.lt/obj/LT-eLABa-0001:E.02~2014~D_20150106_083713-90371.

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There is no doubt that eosinophils and neutrophils are important cells participating in asthma pathogenesis. The most prominent feature reflecting asthma pathogenesis is late-phase airway inflammation, which occurs a few hours after allergen inhalation. The worldwide published studies on asthma show that most attention is paid to individual, not complex, functions of neutrophils and eosinophils in the airways. Moreover, associations between peripheral blood neutrophil and eosinophil activity and infiltration of these cells in the airways during asthma have not been com¬pletely elucidated yet. There are no data about peripheral blood neutrophil and eosinophil activity during allergen-induced late-phase airway inflam¬mation in asthma patients. Therefore, the aim of this study was to evaluate peripheral blood neutrophil and eosinophil functional activity during allergen-induced late-phase airway inflammation in asthma. We found that an inhaled allergen activates peripheral blood neutrophil and eosinophil chemotaxis, phagocytosis, generation of reactive oxygen species and also reduces apoptosis during late-phase airway inflammation in asthma. Furthermore, altered peripheral blood neutrophil and eosinophil functional activity is related with airway neutrophilia and eosinophilia. Our findings provide new evidence about neutrophil and eosinophil functional activity during allergen-induced late-phase airway inflammation in asthma patients.
Mokslininkai neabejoja, jog eozinofilai ir neutrofilai yra vienos svarbiausių ląstelių, dalyvaujančių astmos patogenezėje, kurią labiausiai atspindi vėlyva kvėpavimo takų uždegimo fazė, išsivystanti praėjus kelioms valandoms po alergeno įkvėpimo. Pasaulinėje literatūroje publikuojami darbai, nagrinėja atskirus kvė¬pavimo takų neutrofilų ir eozinofilų aktyvumo pokyčius. Ypač mažai darbų apie periferinio kraujo neutrofilų ir eozinofilų funkcijas bei jų ryšį su šių ląstelių pagausėjimu kvėpavimo takuose, sergant astma. Taip pat nėra tyrimų, vertinančių periferinio kraujo uždegimo ląstelių (neutrofilų ir eozi¬nofilų) funkcijų alergeno sukeltos vėlyvos fazės kvėpavimo takų uždegimo metu. Todėl šio tyrimo tikslas buvo įvertinti periferinio kraujo neutrofilų ir eozinofilų funkcinį aktyvumą alergeno sukeltos vėlyvos fazės kvėpavimo takų uždegimo metu sergant astma. Tyrimo metu nustatėme, kad įkvėptas alergenas aktyvina periferinio kraujo neutrofilų ir eozinofilų funkcijas - chemotaksį, fagocitozę, reaktyvių deguonies formų susidarymą, degranuliaciją bei silpnina apoptozę vėlyvos fazės kvėpavimo takų uždegimo metu. O šių ląstelių aktyvumo pokyčiai yra susiję su kvėpavimo takų neutrofilija ir eozinofilija. Moksliniame darbe pateikiami rezultatai suteikia naujų duomenų apie sergančiųjų alergine astma periferinio kraujo neutrofilų ir eozinofilų funkcinių savybių ypatumus ir parodo jų pokyčius alergeno sukeltos vėlyvos fazes kvėpavimo takų uždegimo metu.
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Shahana, Shahida. "Cell Contacts and Airway Epithelial Damage in Asthma." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4775.

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Books on the topic "Airway eosinophilia"

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Costello, Richard Wilfred Kieran. Recruitment of eosinophils to airway nerves in asthma and in animal models of hyperractivity. 1997.

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Millar, Professor Ann B., Dr Richard Leach, Dr Rebecca Preston, Dr Richard Leach, Dr Richard Leach, Dr Wei Shen Lim, Dr Richard Leach, et al. Respiratory diseases and respiratory failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199565979.003.0005.

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Chapter 5 covers respiratory diseases and respiratory failure, including clinical presentations of respiratory disease, assessment of diffuse lung disease, hypoxaemia, respiratory failure, and oxygen therapy, pneumonia, mycobacterial infection, asthma, chronic obstructive pulmonary disease (COPD), lung cancer, mediastinal lesions, pneumothorax, pleural disease, asbestos-related lung disease, diffuse parenchymal (interstitial) lung disease, sarcoidosis, pulmonary hypertension, acute respiratory distress syndrome, bronchiectasis and cystic fibrosis, bronchiolitis, eosinophilic lung disease, airways obstruction, aspiration syndromes, and near-drowning, pulmonary vasculitis, the immunocompromised host, sleep apnoea, and rare pulmonary diseases.
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Book chapters on the topic "Airway eosinophilia"

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Schellenberg, R. R. "Pharmacologic Modulation of Antigen-induced Airway Eosinophilia and Hyperresponsiveness in Guinea Pigs." In New Concepts in Asthma, 50–64. London: Macmillan Education UK, 1993. http://dx.doi.org/10.1007/978-1-349-12673-6_5.

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Dhariwal, Jaideep, Yorissa Padayachee, and Sebastian L. Johnston. "Respiratory viruses and eosinophilic airway inflammation." In Eosinophilic Lung Diseases, 204–18. Sheffield, United Kingdom: European Respiratory Society, 2022. http://dx.doi.org/10.1183/2312508x.10030120.

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De La Torre, Ubaldo, Allison D. Fryer, David B. Jacoby, and Matthew G. Drake. "Eosinophils and airway nerves in asthma." In Eosinophilic Lung Diseases, 193–203. Sheffield, United Kingdom: European Respiratory Society, 2022. http://dx.doi.org/10.1183/2312508x.10029320.

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Ueki, Shigeharu, Yuma Fukutomi, Yui Miyabe, Takechiyo Yamada, Tsuyoshi Oguma, and Koichiro Asano. "Allergic fungal diseases in the upper and lower airways." In Eosinophilic Lung Diseases, 119–40. Sheffield, United Kingdom: European Respiratory Society, 2022. http://dx.doi.org/10.1183/2312508x.10030020.

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Coyle, Anthony J., and Jose Carlos Gutierrez-Ramos. "Eosinophils in asthma." In Cellular Mechanisms in Airways Inflammation, 147–58. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8476-1_5.

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Butchers, P. R., and C. J. Vardey. "The Effect of Prostanoids on the Function of Human Eosinophils." In Mediators in Airway Hyperreactivity, 103–12. Basel: Birkhäuser Basel, 1990. http://dx.doi.org/10.1007/978-3-0348-7379-6_12.

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Sedgwick, Julie B., and William W. Busse. "Adhesion Proteins on Airway Eosinophils in Allergy and Asthma." In New Drugs in Allergy and Asthma, 163–72. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-7324-6_14.

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Carlos Herrera Garcia, Jose. "Eosinophils as a Biomarker in Asthma and COPD." In Update in Respiratory Diseases. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.94240.

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Asthma and COPD are two diseases related to eosinophils. But at present, we do not know with certainty how much these cells participate in these diseases, beyond that the treatment of the underlying cause produces the resolution of eosinophilia in a “reactive” way. Eosinophil-related diseases are a spectrum of systemic diseases such as Asthma and COPD in pneumology area. Under inflammatory conditions, the number of circulating eosinophils or tissues can increase dramatically, with rapid development of eosinophilia and we can obtain in a simple laboratory test. In general, the number of eosinophils in the blood can provide useful information and considering the differential diagnosis and for the subsequent test of patients presenting with eosinophilia. The treatment of eosinophilia currently in number of 300 cells in which is the criteria and the target to be treat. The best known and most used of all treatments for diseases related to eosinophils are corticosteroids, which decrease circulating and tissue eosinophils in a few hours, through mechanisms that include the direct activation of eosinophil program death. Targeted treatment against eosinophils could improve airway remodeling through mechanisms that are not fully known, and their effects on lung function are variable and decreasing symptoms in patients.
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Maytham Hameed, Raghdah, Haidar Abdul Amir Najim Abood, and Mohanad Mohsin Ahmed. "Interleukin-5 and Interleukin-5 Receptor Polymorphism in Asthma." In Chemokines Updates [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105078.

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Asthma is a common chronic inflammatory disease of the airways of the lungs, in the world. It’s associated with type 2 cytokines interleukin-4, IL-5, and IL-13, which promote airway eosinophilia, bronchial hyperresponsiveness, mucus overproduction, and immunogloubulin E synthesis. IL-5 is a cytokine known to play major role in the regulation of eosinophil formation, maturation, survival, and recruitment. Hence, an increased production of IL-5 may be contributed to the pathogenesis of asthma. The expression of human IL-5 receptor presented on eosinophils, basophils, and mast cells. Hence, a polymorphism in IL-5 receptor may be implicated in the development of asthma. Many candidate genes that could potentially contribute to the susceptibility to the disease have not been investigated to date, and not all of the polymorphisms of the candidate genes have been tested for a possible association with the disease. Taking this into consideration, IL-5 (together with the IL-5 receptor) polymorphism deserves attention as the subject of further investigations into asthma. In this review, we will address the role of IL-5 and IL-5 receptor polymorphism in asthma, describe the impact of these polymorphisms on the Blood parameters and clinical parameters. Further, give an overview of preclinical and clinical studies targeting the IL-5 and IL-5 receptor pathway.
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Kume, Hiroaki, Ryuki Yamada, and Yuki Sato. "New Perspectives in Pharmacological Therapy for COPD: Phenotype Classification and Corticosteroids with Bronchodilators." In Chronic Obstructive Pulmonary Disease - A Compendium of Medicine and the Humanities [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106949.

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Chronic obstructive lung disease (COPD) is heterogeneous and complex. Symptoms and pathophysiological disorders overlap between COPD and asthma. To progress the management of COPD, patients with COPD should be classified by distinct clinical phenotypes. These groupings derived from multiple dimensions including clinical, physiologic, imaging, and endotyping determine clusters of patients with common characteristics that relate to clinically meaningful outcomes such as symptoms, exacerbations, response to therapy, and disease progression (stratified medicine). Moreover, since several phenotypes can coexist in individual patients with COPD, an approach due to therapeutic target identified phenotypes and endotypes (treatable traits) has been proposed as an advanced therapy recently (precision medicine). Airway eosinophilia and airway hyperresponsiveness, which are hallmarks of asthma, are developed in some patients with COPD, independent of asthma. It is perhaps meaningful to classify COPD according to airway eosinophilia and airway hyperresponsiveness as phenotypes and to put these phenotypes into focus as treatable traits. These phenotypes are closely related to frequency of exacerbations and reactivity to inhaled corticosteroids with bronchodilators in therapy for COPD. Hence, research for phenotype classification can play a fundamental role for development of the management and treatment for COPD.
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Conference papers on the topic "Airway eosinophilia"

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James, Wai Yee, Claire Greiller, Beverley MacLaughlin, Neil Barnes, Raj Rajakulasingam, Angshu Bhowmik, Aklak Choudhury, et al. "Peripheral blood eosinophilia predicts lower airway eosinophilia in asthma and COPD." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3881.

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Colangelo, M., A. Llop-Guevara, R. Fattouh, TD Walker, S. Goncharova, M. Lovric, and M. Jordana. "Modeling of HDM-Induced Chronic Airway Eosinophilia." 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.a4233.

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Larkin, Allyson S., Samuel A. Yousem, and Sally E. Wenzel. "Small Airway Obstruction, Eosinophilia And Airway Granulomas: A New Phenotype Of Severe Asthma?" 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.a3723.

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Colangelo, Marc, Alba Llop-Guevara, Ramzi Fattouh, Tina D. Walker, Susanna Goncharova, Miroslav Lovric, and Manel Jordana. "Modeling Of House Dust Mite-Induced Chronic Airway Eosinophilia." 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.a2806.

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Kume, Hiroaki, Masayuki Hojo, and Naozumi Hashimoto. "Involvement of airway eosinophilia and airway hyperresponsiveness in management and therapy for COPD>." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.985.

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Murphy, GE, NI Pitman, M. Kurowska-Stolarska, P. Kewin, D. Xu, C. McSharry, NC Thomson, and MC Shepherd. "Murine Airway Eosinophilia Following IL-33 Administration Is Eotaxin Dependent." 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.a4253.

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Takeyama, Kiyoshi, Tomohiro Akaba, Atsushi Kurokawa, Ken Arimura, Mitsuko Kondo, and Etsuko Tagaya. "Analysis of airway mucin concentration in patients with pulmonary eosinophilia." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4390.

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Silberbrandt, Alexander, Anna Von Bülow, Vibeke Backer, and Celeste Porsbjerg. "Airway eosinophilia in severe asthma is associated with smoking history." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa948.

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Whitman-Purves, Emily M., John B. Trudeau, and Sally E. Wenzel. "Airway Epithelial Eosinophilia Is Associated With Asthma And Better Predicts Severity Than Sputum Or BAL Eosinophils." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3935.

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O'Sullivan, Jenna, Liam Chawke, Deirdre Fitzgerald, David Curran, and Terry O'Connor. "Small airways disease and peripheral eosinophilia predict airway hyperresponsiveness in Irish patients with suspected asthma." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa5024.

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