Relevant bibliographies by topics / Allergic Airways Disease

Academic literature on the topic 'Allergic Airways Disease'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 January 2023

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Journal articles on the topic "Allergic Airways Disease"

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Lew, D. Betty, Kim S. LeMessurier, Maneesha Palipane, Yanyan Lin, and Amali E. Samarasinghe. "Saccharomyces cerevisiae-Derived Mannan Does Not Alter Immune Responses to Aspergillus Allergens." BioMed Research International 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/3298378.

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Severe asthma with fungal sensitization predominates in the population suffering from allergic asthma, to which there is no cure. While corticosteroids are the mainstay in current treatment, other means of controlling inflammation may be beneficial. Herein, we hypothesized that mannan from Saccharomyces cerevisiae would dampen the characteristics of fungal allergic asthma by altering the pulmonary immune responses. Using wild-type and transgenic mice expressing the human mannose receptor on smooth muscle cells, we explored the outcome of mannan administration during allergen exposure on the pathogenesis of fungal asthma through measurement of cardinal features of disease such as inflammation, goblet cell number, and airway hyperresponsiveness. Mannan treatment did not alter most hallmarks of allergic airways disease in wild-type mice. Transgenic mice treated with mannan during allergen exposure had an equivalent response to non-mannan-treated allergic mice except for a prominent granulocytic influx into airways and cytokine availability. Our studies suggest no role for mannan as an inflammatory regulator during fungal allergy.
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Morianos, Ioannis, and Maria Semitekolou. "Dendritic Cells: Critical Regulators of Allergic Asthma." International Journal of Molecular Sciences 21, no. 21 (October 26, 2020): 7930. http://dx.doi.org/10.3390/ijms21217930.

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Allergic asthma is a chronic inflammatory disease of the airways characterized by airway hyperresponsiveness (AHR), chronic airway inflammation, and excessive T helper (Th) type 2 immune responses against harmless airborne allergens. Dendritic cells (DCs) represent the most potent antigen-presenting cells of the immune system that act as a bridge between innate and adaptive immunity. Pertinent to allergic asthma, distinct DC subsets are known to play a central role in initiating and maintaining allergen driven Th2 immune responses in the airways. Nevertheless, seminal studies have demonstrated that DCs can also restrain excessive asthmatic responses and thus contribute to the resolution of allergic airway inflammation and the maintenance of pulmonary tolerance. Notably, the transfer of tolerogenic DCs in vivo suppresses Th2 allergic responses and protects or even reverses established allergic airway inflammation. Thus, the identification of novel DC subsets that possess immunoregulatory properties and can efficiently control aberrant asthmatic responses is critical for the re-establishment of tolerance and the amelioration of the asthmatic disease phenotype.
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KRISHNA, M. T., I. MUDWAY, F. J. KELLY, A. J. FREW, and S. T. HOLGATE. "Ozone, airways and allergic airways disease." Clinical Experimental Allergy 25, no. 12 (December 1995): 1150–58. http://dx.doi.org/10.1111/j.1365-2222.1995.tb03037.x.

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Carlsten, Chris, Anders Blomberg, Mandy Pui, Thomas Sandstrom, Sze Wing Wong, Neil Alexis, and Jeremy Hirota. "Diesel exhaust augments allergen-induced lower airway inflammation in allergic individuals: a controlled human exposure study." Thorax 71, no. 1 (November 16, 2015): 35–44. http://dx.doi.org/10.1136/thoraxjnl-2015-207399.

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RationaleTraffic-related air pollution has been shown to augment allergy and airway disease. However, the enhancement of allergenic effects by diesel exhaust in particular is unproven in vivo in the human lung, and underlying details of this apparent synergy are poorly understood.ObjectiveTo test the hypothesis that a 2 h inhalation of diesel exhaust augments lower airway inflammation and immune cell activation following segmental allergen challenge in atopic subjects.Methods18 blinded atopic volunteers were exposed to filtered air or 300 µg PM2.5/m3 of diesel exhaust in random fashion. 1 h post-exposure, diluent-controlled segmental allergen challenge was performed; 2 days later, samples from the challenged segments were obtained by bronchoscopic lavage. Samples were analysed for markers and modifiers of allergic inflammation (eosinophils, Th2 cytokines) and adaptive immune cell activation. Mixed effects models with ordinal contrasts compared effects of single and combined exposures on these end points.ResultsDiesel exhaust augmented the allergen-induced increase in airway eosinophils, interleukin 5 (IL-5) and eosinophil cationic protein (ECP) and the GSTT1 null genotype was significantly associated with the augmented IL-5 response. Diesel exhaust alone also augmented markers of non-allergic inflammation and monocyte chemotactic protein (MCP)-1 and suppressed activity of macrophages and myeloid dendritic cells.ConclusionInhalation of diesel exhaust at environmentally relevant concentrations augments allergen-induced allergic inflammation in the lower airways of atopic individuals and the GSTT1 genotype enhances this response. Allergic individuals are a susceptible population to the deleterious airway effects of diesel exhaust.Trial registration numberNCT01792232.
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TODEA, Doina Adina, Iuliu SUATEAN, Andreea Codruta COMAN, and Loredana Elena ROSCA. "The Effect of Climate Change and Air Pollution on Allergenic Potential of Pollens." Notulae Botanicae Horti Agrobotanici Cluj-Napoca 41, no. 2 (December 6, 2013): 646. http://dx.doi.org/10.15835/nbha4129291.

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Climate change is associated with atmospheric warming due to continuous increase in anthropogenic greenhouse gas concentration following the industrial revolution. The urban areas are more responsible for these changes. Europe for example has experienced a progressive warming +0.9°C for 1901-2005. Climate change is unequivocal and represents a possible threat for patients affected by allergic conditions because it is related with an increased distribution and concentration of pollen. Higher temperature, wet condition (especially thunderstorms), wind speed, transition of cold fronts, environmental changes (allergenic pollens arrived in new areas), are mechanisms which involve changes of production, dispersion and allergen content of pollen. Prolonged and more severe pollen seasons are leading to worsened asthma and allergies. The interaction of pollen with urban air pollutants could also lead to an increased effect of aero allergens on allergic patients, with a greater likelihood of the development of an allergic respiratory disease in sensitized subjects and exacerbation of symptomatic patients. Air pollution could induce damage to airways mucosa, thus promoting sensitization of the airways; also it could increase the expression of allergenic proteins (allergen contents of pollen produce by plants is increased by higher temperature and CO2 enriched atmosphere). By increasing pollen concentration or making the airways susceptible to allergens, the climate change and air pollution have a negative impact on human health.
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Haberal, Ilknur, and Jacquelynne P. Corey. "The Role of Leukotrienes in Nasal Allergy." Otolaryngology–Head and Neck Surgery 129, no. 3 (September 2003): 274–79. http://dx.doi.org/10.1016/s0194-5998(03)00601-6.

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OBJECTIVE: This review focuses on the role of cysteinyl leukotrienes (cysLTs) in nasal allergy. The purpose was to provide knowledge of the role of cysLTs in the pathophysiology of nasal allergy and the role of antileukotrienes in the treatment of nasal allergies. MATERIALS AND METHODS: We conducted a literature review. RESULTS: The proinflammatory effects of cysLTs have been well described in asthma. Antileukotrienes have proved to be an effective anti-inflammatory treatment for asthma patients. Similar to pathogenesis of asthma, cysLTs exert potent inflammatory effects in the upper airways and play a role in the pathogenesis of allergic rhinitis and other nasal allergies. CONCLUSION: Antileukotriene treatment appears to be beneficial in nasal allergies. Allergic rhinitis is a complex, IgE-mediated inflammatory disease of the upper airways. It is the most common allergic disease, occurring in 10% to 30% of adults and up to 30% of children. It may be perennial or seasonal. Sneezing, itching, watery rhinorrhea, and nasal obstruction are classic symptoms. It may impair cognition, school/work performance and productivity, behavior, mood, and quality of life. On physical examination, clear secretions, nasal congestion, pink-bluish nasal mucosa, the allergic salute, and allergic shiners may be detected. Allergic rhinitis is a common comorbid condition with asthma, sinusitis, otitis media, nasal polyposis, and respiratory infections.
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Salvador, Laia Castro, Christabelle Chen, and Runa Ali. "Allergic rhinitis and its impact on airways disease." Practice Nursing 33, no. 4 (April 2, 2022): 138–44. http://dx.doi.org/10.12968/pnur.2022.33.4.138.

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Allergic rhinitis is linked to an increased risk of asthma development. Laia Castro Salvador et al discuss the impact of allergic rhinitis and how it can be managed Allergic rhinitis is characterised by symptoms including rhinorrhoea, sneezing, nasal obstruction and itching, which have a great impact on the patient's quality of life. Allergic rhinitis can be classified depending on the frequency and severity of symptoms, and can be sub-divided into seasonal and perennial. Allergic rhinitis is linked to an increased risk of asthma development and both diseases are believed to be different expressions of the same inflammatory process. The aim of the treatment is improving the patient's quality of life by relieving symptoms. Management of allergic rhinitis will encompass a combination of allergen avoidance, pharmacological therapies and patient education and adherence.
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Redington, Anthony E., and Peter H. Howarth. "Mast Cells, Cytokines and Asthma." Canadian Respiratory Journal 1, no. 2 (1994): 118–27. http://dx.doi.org/10.1155/1994/435781.

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The appreciation that asthma is a chronic inflammatory disorder of the airways has led to a reappraisal of the importance of different cell populations within the bronchial mucosa with respect to their role in the regulation of the cellular events in this disease. While mast cell degranulation has been implicated in the acute allergic bronchoconstrictor response, activation of this cell population has not been considered relevant to either the late phase inflammatory cell influx within the airways following allergen bronchoprovocation or to the mucosa! eosinophilia in chronic clinical disease. As such, attention has focused on the T lymphocyte as an orchestrator of these cellular events on account of its ability to synthesize and release cytokines relevant to the allergic process. It is now, however, realized that many cell populations within the airways are able to generate cytokines comparable with and complimentary to those produced by T lymphocytes and that asthma cannot be considered an inflammatory airway disorder dependent upon activation of one single cell population. This review details the current evidence that airway mast cells synthesize, store and release cytokines relevant to allergic inflammation and considers their potential involvement not only in the cellular influx within the airways but also in the fibrotic structural changes which are evident in chronic disease.
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Haccuria, Amaryllis, Alain Van Muylem, Andrei Malinovschi, Vi Doan, and Alain Michils. "Small airways dysfunction: the link between allergic rhinitis and allergic asthma." European Respiratory Journal 51, no. 2 (February 2018): 1701749. http://dx.doi.org/10.1183/13993003.01749-2017.

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Abnormal airway reactivity and overproduction of nitric oxide (NO) occurring in small airways have been found in asthma. If the “one airway, one disease” concept is consistent, such dysfunctions should also be detected in the peripheral airways of patients suffering from allergic rhinitis.We investigated whether peripheral airway reactivity and NO overproduction could be documented in distal airways in patients with allergic rhinitis. Exhaled NO fraction (FeNO) and the slope (S) of phase III of the single-breath washout test (SBWT) of helium (He) and sulfur hexafluoride (SF6) were measured in 31 patients with allergic asthma, 23 allergic rhinitis patients and 24 controls, before and after sputum induction. SBWT is sensitive to airway calibre change occurring in the lung periphery.The FeNO decrease was more significant in asthma and rhinitis than in controls (−55.1% and −50.0%, respectively, versus −40.8%) (p=0.007 and p=0.029, respectively). SSF6 and SHe increased in all groups. Change in SHe (ΔSHe) > ΔSSF6 was observed in rhinitis (p=0.004) and asthma (p<0.001), whereas ΔSSF6 = ΔSHe in controls (p=0.431).This study provides evidence of peripheral airway dysfunction in patients with allergic rhinitis quite similar to that described in asthma. Furthermore, a large proportion of the increased NO production reported in allergic rhinitis appears to originate in the peripheral airways.
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Jaffar, Zeina, Maria Ferrini, and Kevan Roberts. "Pulmonary NK cells prevent allergic airway sensitization: Regulation by CB2 cannabinoid receptors." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 192.6. http://dx.doi.org/10.4049/jimmunol.196.supp.192.6.

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Abstract Allergic asthma is a chronic inflammatory disease involving the interaction between the innate and adaptive immune response. Endogenously generated cannabinoids, acting via CB receptors play important roles in both homeostatic and inflammatory processes. CB2-active compounds are known to impact innate immunity including responses by monocytes and NK cells. However, the contribution of pulmonary NK cells and CB2-active endocannabinoids to the innate events preceding sensitization of the airways to the common house dust mite (HDM) allergen is unclear. We investigated the significance of CB2 activation during allergen-triggered pulmonary inflammation and NK cell effector function. Allergic airway inflammation was induced in mice by sensitization via the airways by intranasal HDM instillation, and responses in wild type (WT) and CB2-deficient (CB2−/−) mice were compared. Mice lacking CB2 receptor exhibited elevated numbers of pulmonary NK cells yet were resistant to the induction of allergic inflammation and showed diminished airway hyperreactivity, pulmonary eosinophilia, TH2 cytokine production and mucus secretion after allergen inhalation. Cellular depletion and adoptive transfer studies were undertaken to dissect the mechanisms involved. Depletion of NK cells restored HDM responsiveness. Conversely, transfer of CB2−/− NK cells into WT mice suppressed the allergic airway inflammation and was associated with a reduction in monocyte-derived dendritic cells but elevated CX3CL1 release and recruitment of Ly6C−CX3CR1+ monocytes. These studies established a crucial role for CB2 activation in allergic lung disease via regulation of NK cell function and identified novel therapeutic targets for treatment of asthma.
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Dissertations / Theses on the topic "Allergic Airways Disease"

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Limbrey, Rachel Mary. "Epithelial repair in allergic airways disease." Thesis, University of Southampton, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403829.

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Wilson, Andrew M. "Anti-inflammatory therapy in allergic airways disease." Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/23268.

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The system adverse effects of inhaled corticosteroids were investigated in dose-response studies. By measuring cortisol suppression, it was shown that a more potent inhaled corticosteroid (fluticasone propionate (FP)) exhibits greater systemic bioactivity (2-fold at highest licensed doses) than a weaker steroid (triamcinolone acetonide (TAA)). No differences were detected between inhaled corticosteroids of similar potency (TAA and flunisolide), even when using sensitive and novel measures e.g. low dose ACTH stimulation and early morning urine cortisol excretion. The latter test may prove to have clinical implications for monitoring patients, as it was shown to be more sensitive than dynamic or basal serum cortisol measures. However, the lung delivery of a corticosteroid has a greater effect on systematic bioactivity than its dose or potency, as the systematic activity of FP via two different inhaler devices was shown to vary more than 4-fold. Studies comparing oral prednisolone with inhaled FP, showed FP to exhibit dose-related suppression of serum cortisol in a 1:8.5mg ratio compared to prednisolone. Interestingly, the effects of FP on markers of bone metabolism were less marked than adrenal suppression, compared to the effects of prednisolone. Intra-nasal FP also produced significant urinary cortisol suppression, whereas other intra-nasal corticosteroids (TAA, budesonide (BUD), beclomethasone, mometasone) had no significant effects on 24 hour cortisol, bone or blood markers. Furthermore, the addition of intranasal to inhaled FP resulted in more patients with sub-normal cortisol values. A meta-analysis of all dose-response studies assessing different inhaled corticosteroids was also performed with results supporting this data. When assessing therapeutic effects of inhaled corticosteroids, it was shown that a lower dose of BUD was required to optimise symptoms, lung function and exhaled nitric oxide (eNO), compared to other measures of inflammation; serum markers (ECP), and bronchial hyperreactivity to adenosine monophosphate (AMP) and methacholine.
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MacKenzie, Karen Joan. "Peptide immunotherapy in models of allergic airways disease." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5911.

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Allergen-reactive CD4+ T cells are implicated in the pathogenesis of allergic disease. Peptide immunotherapy (PIT) involves therapeutic administration of short immunodominant peptides from within the protein allergen to which CD4+ T cell responses are directed. This approach can induce tolerance of allergen-reactive CD4+ T cells, while negating the risk of severe allergic reactions associated with whole allergen specific immunotherapy. PIT therefore holds promise as a diseasemodifying treatment for allergic patients. However, further information regarding the mechanisms of action of PIT are required to aid translation to the allergy clinic. Chicken ovalbumin (OVA) is a commonly used model allergen in mouse models of allergic airways inflammation (AAI). Trackable, T cell receptor transgenic T cells recognizing the immunodominant 323-339 peptide of OVA (pOVA) allow mechanistic investigation of PIT in response to pOVA. This thesis investigated the hypothesis that strong, systemic T cell responses induced by intravenous administration of soluble pOVA will induce i) tolerance to pOVA and ii) linked suppression to any additional OVA T cell epitopes, hence improving OVA-induced AAI. Contrary to the hypothesis, intravenous pOVA PIT did not improve disease in a C57BL/6 model of OVA-induced AAI. Models of OVA-induced allergic sensitisation and AAI were therefore developed incorporating trackable CD4+ pOVA-reactive T cells (OT-II cells). pOVA PIT induced tolerance of these cells in an allergic sensitisation setting, but had limited impact on the overall OVA response. Yet, in a model of AAI driven solely by Th2 polarised CD4+ OT-II cells, pOVA PIT did improve disease. It was concluded that, in non-transgenic C57BL/6 mice, CD4+ T cells responding to additional epitope(s) within OVA were important in driving disease and that these T cells were not subject to linked suppression following pOVA PIT. Using a panel of overlapping peptides constituting the sequence of OVA, a novel CD4+ epitope within OVA was characterised. The effects of PIT using pOVA in combination with a peptide containing this additional epitope on OVA-induced AAI were then assessed. Findings from this project therefore hold importance for future mechanistic work surrounding PIT in allergic disease.
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Choo-Kang, Brian Shù Wing. "Modulation of inflammatory pathways in allergic airways disease." Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433047.

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Gould, David James. "Leucocyte recruitment in a model of allergic airways disease." Thesis, University of Southampton, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384947.

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Varley, John Graeme. "Development of a model of allergic airways disease A." Thesis, University of Southampton, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385226.

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Peel, Tamlyn Jolyon Robert. "IL-17 modulation of rhinovirus-induced allergic airways disease." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/18999.

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Asthma is a chronic inflammatory disease of the airways, resulting in significant morbidity and premature deaths. Rhinoviruses, agents of the common cold, have been identified as the most frequent viruses inducing asthma exacerbations. However the mechanisms involved in this process, especially in moderate-to-severe asthmatics, are not clear. IL-17, a protein secreted by Th17 and IL-17+γδ T cells, is found to be up-regulated in asthmatics and correlates with severity of disease. Observations from a clinical study of rhinovirus infection showed increased induction of IL-17 in nasal lavage fluid from asthmatics following experimental rhinovirus infection compared to healthy controls. Using mouse models, this thesis addresses the interactions of rhinovirus with IL-17 in the context of allergic airways disease. Primary infection of C57BL/6 mice did not induce IL-17 responses as seen in human subjects; this may be explained by the apparent lack of induction of IL-23 following primary infection in mice. Supplementation of rhinovirus infection with recombinant IL-17 showed significant, selective increases in neutrophil chemokines with subsequent increases in both neutrophil recruitment and activation, as defined by myeloperoxidase activity. In an existing Th2-driven model of allergic airways disease, rhinovirus was seen to selectively expand Th2 responses while not increasing allergen-induced Th17, IL-17+γδ T cells or IL-17. However, rhinovirus infection in a Th17-driven model of allergic airways disease showed a significant increase of neutrophil numbers with a concomitant increase in airway hyperresponsiveness. This work augments existing knowledge on rhinovirus exacerbation of Th2-mediated asthma with the interactions between Th17 and rhinovirus, which may play a significant role in moderate-to-severe asthma exacerbations. This supports current research on therapeutic targeting of the IL-17 pathway in asthmatics.
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Mathie, Sara A. "Mechanisms underlying the resolution of HDM induced allergic airways disease." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/29879.

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Allergic asthma is a chronic inflammatory disease of the lung and deficiencies in pro-resolving mechanisms may contribute to the persistence of inflammation. The overall aim of this project was to establish a resolution model of house dust mite (HDM) induced allergic airway disease (AAD) and identify mediators of resolution. In our model, features of disease, induced by HDM at peak disease 4 hours, airway hyper-reactivity (AHR), Th2 lymphocytes and eosinophils remained significantly elevated 7 days after last challenge, resolving to baseline by 13 days. The levels of FoxP3+ regulatory lymphocytes also follow this pattern. However, as disease waned there was an elevation in the levels of alveolar macrophages and up regulation of the homeostatic molecule CD200R up to 13 days. Exposure to a single i.n administration of HDM in the resolved airways resulted in a rapid increase in Th2 inflammation and AHR suggesting that after resolution of HDM inflammation there is altered immune homeostasis in the lung. The pro-resolving lipid Lipoxin A4 was induced in the lung by HDM exposure and remained detectable during resolution. Depletion of alveolar macrophages during the resolution phase of allergen challenge resulted in delayed clearance of Th2 lymphocytes, airway neutrophils and interstitial macrophages. Conversely, adoptive transfer of alveolar macrophages during resolution resulted in reduced numbers of lung tissue leukocytes, specifically neutrophils and interstitial macrophages. This suggests a cross talk between these macrophage subsets and a novel interaction for pulmonary homeostasis. The anti-inflammatory peptide Annexin A1 is highly expressed by alveolar macrophages and mice deficient in Annexin A1 had enhanced AHR and Th2 immunity response to HDM. Blocking the Annexin A1 receptor FPR2 enhanced AHR and lung inflammation. Conversely, therapeutic administration of an Annexin A1 mimetic improved AHR and Th2 immunity. These studies demonstrate that Annexin A1: FPR2 pathway may be important in HDM disease and that resolution of allergic airways disease is an active process resulting in altered homeostasis of the lung.
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Kearley, Jennifer. "Manipulation of Th2 cell function in allergic airways disease in vivo." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430819.

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Pitman, Nicholas Ian. "The role of IL-33 and ST2 in allergic airways disease." Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/1817/.

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Asthma is a chronic disease characterised by variable airflow obstruction, bronchial hyperresponsiveness and airways inflammation. At an immunological level Th2 inflammation and the presence of activated eosinophils and mast cells are key features of asthma. ST2, the receptor for the novel cytokine IL-33, is expressed upon Th2 lymphocytes and mast cells but its role in clinical and experimental asthma remains unclear. IL-33 has been shown to induce local and systemic eosinophilia when administered to the peritoneum of mice. In this thesis I have set out to test the hypothesis that the activation of mast cells by IL-33 acting on cell surface ST2 plays a critical role in allergic airways inflammation. I began by studying the function of ST2 on mast cells in vitro. I found that ST2 was expressed at an early stage of development, and correlated closely with the expression of the stem cell factor receptor (c-kit), a marker present on mast cells from a progenitor stage. Despite this mast cells generated form ST2 gene deleted mice proliferated and matured normally. When mast cells were activated by IL-33, acting in an ST2-dependent manner, pro-inflammatory cytokines and chemokines were released that have potential roles in asthma, specifically IL-6, IL-13, MIP-1α and MCP-1. To extend these findings I looked at the role of ST2 in allergic airways inflammation. I first optimised and validated an ovalbumin and adjuvant based ‘short’ twelve day model of murine asthma and demonstrated that ST2 gene deletion results in attenuated eosinophilic inflammation. In addition to being ST2 dependent it is possible that this adjuvant based short model is mast cell dependent, unlike longer adjuvant based models which are mast cell and ST2 independent. Therefore I went on to study an adjuvant-free model of asthma which has been demonstrated to be mast cell dependent. In this adjuvant-free model of asthma the airway inflammation was attenuated in ST2 gene deficient mice compared with wild type mice, while AHR was unaffected. There was an associated reduction in IgE production and thoracic lymph node recall Th2 cytokine responses. I then examined the effect of ST2 activation in the lungs. When IL-33 was administered directly to the airways of naïve mice it induced the features of experimental asthma. There was extensive eosinophilic inflammation within the lung tissue and airspaces. The Th2 cytokines IL-5 and IL-13, and the eosinophil chemoattractant chemokines eotaxin-1 and eotaxin-2 were detected at increased concentrations. Significant airways hyperresponsiveness was also generated. Using ST2 gene deleted mice I demonstrated that these effects were ST2 specific. Although I have shown that mast cells are activated by IL-33 in vitro, I used mast cell deficient mice to demonstrate that the eosinophilic inflammation generated by IL-33 is unaffected by the absence of mast cells. These data show that IL-33 can induce in the lungs the cardinal pathological characteristics of asthma, and that it appears to act upstream of other important mediators such as IL-13 and the eotaxins. Furthermore the IL-33 receptor ST2 is required in an adjuvant free model of asthma, which is more akin to human disease. Placing these findings in the context of recent evidence that IL-33 is released by structural cells in response to damage or injury suggests that IL-33 may play a key role in initiating the immunological features of clinical asthma. As a consequence of this position in the hierarchy of inflammation IL-33 offers a promising direct target for novel biological therapies in asthma.
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Books on the topic "Allergic Airways Disease"

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Cullinan, Paul, and Joanna Szram. Occupational lung disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0142.

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Some occupational lung diseases are defined by their clinical or pathological nature (e.g. occupational asthma or mesothelioma), while others are defined by their specific etiology (e.g. silicosis, farmer’s lung). Most fall into one of three categories. The first is airways disease, including occupational asthma (induced by a workplace agent), work-exacerbated asthma (preexisting asthma provoked by one or more agents at work), and irritant-induced asthma (initiated by a single, toxic exposure to a respiratory irritant); COPD and obliterative bronchiolitis may arise from workplace exposures, and around 10% of lung cancers have an occupational etiology. The second is parenchymal diseases, incorporating the many types of pneumoconiosis, differentiated by the dust that caused them, and the many types of extrinsic allergic alveolitis (or hypersensitivity pneumonia) categorized by the occupations in which they arise. The third is pleural diseases comprising pleural plaques, diffuse pleural thickening, and mesothelioma.
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Duong-Quy, Sy, ed. Allergic Rhinosinusitis and Airway Diseases. MDPI, 2022. http://dx.doi.org/10.3390/books978-3-0365-4815-9.

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Airway and Exercise, an Issue of Immunology and Allergy Clinics of North America. Elsevier - Health Sciences Division, 2018.

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Frew, Anthony. Air pollution. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0341.

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Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.
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Gilchrist, Francis J., and Alex Horsley. Management of respiratory exacerbations. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0005.

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Cystic fibrosis lung disease is characterized by chronic infection, inflammation and a progressive loss of lung function. Patients are also affected by recurrent episodes of increased respiratory symptoms, called exacerbations which have a detrimental effect on quality of life, the rate of lung function decline, and mortality. Early diagnosis and treatment is vital. Diagnosis relies on a combination of symptoms, examination findings, the results of laboratory tests, and lung function. Antibiotics are the mainstay of treatment but airway clearance, nutrition, and glucose homeostasis must also be optimized. Mild exacerbations are usually treated with oral antibiotics and more severe exacerbations with intravenous antibiotics. The choice of antibiotic is guided by the patient’s chronic pulmonary infections, the in-vitro antibiotic sensitivities, known antibiotic allergies, and the previous response to treatment. In patients with chronic Pseudomonas aeruginosa infection, antibiotic monotherapy is thought to increase the risk of resistance and treatment with 2 antibiotics is therefore suggested (usually a β‎-lactam and an aminoglycoside). Although there is a lack of evidence on the duration of treatment, most patients receive around 14 days. This can be altered according to the time taken for symptoms and lung function to return to pre-exacerbation levels. If patients are carefully selected and receive appropriate monitoring, home intravenous antibiotics can be as effective as in-patient treatment. They are also associated with decreased disruption to patients / family life, decreased risk of cross infection and decreased costs.
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Book chapters on the topic "Allergic Airways Disease"

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Natarajan, Prabitha, Linda A. Guernsey, and Craig M. Schramm. "Regulatory B Cells in Allergic Airways Disease and Asthma." In Methods in Molecular Biology, 207–25. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1161-5_15.

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Harkema, Jack R., and James G. Wagner. "Non-Allergic Models of Mucous Cell Metaplasia and Mucus Hypersecretion in Rat Nasal and Pulmonary Airways." In Mucus Hypersecretion in Respiratory Disease, 181–200. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470860790.ch12.

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Allen, Irving C. "Induction of Allergic Airway Disease Using House Dust Mite Allergen." In Methods in Molecular Biology, 159–72. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-496-8_13.

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Gerber, Vinzenz. "Recurrent Airway Obstruction and Inflammatory Airway Disease." In Veterinary Allergy, 371–83. Oxford, UK: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118738818.ch55.

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Meyer-Martin, Helen, Sebastian Reuter, and Christian Taube. "Mouse Models of Allergic Airway Disease." In Methods in Molecular Biology, 127–41. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1212-4_13.

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Ramsay, Alistair J., Simon P. Hogan, Paul S. Foster, and Yelin Xiong. "Cytokine gene therapy of allergic airways inflammation." In Gene Therapy in Inflammatory Diseases, 65–81. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8478-5_5.

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Lukacs, Nicholas W. "The Role of Chemokines in Allergic Airway Inflammation." In Chemokines in Disease, 111–21. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-706-2_7.

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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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Oh, Chad K. "Mast Cell Mediators in Airway Remodeling." In Mast Cells in Allergic Diseases, 85–100. Basel: KARGER, 2005. http://dx.doi.org/10.1159/000087573.

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Jacobs, Ruth, and Michael Kaliner. "Current Concepts of the Pathophysiology of Allergic Asthma." In Airway Smooth Muscle in Health and Disease, 277–99. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0779-2_14.

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Conference papers on the topic "Allergic Airways Disease"

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Saglani, Sejal, Carla P. Jones, Stephen Lui, Simone Walker, Andrew Bush, and Clare M. Lloyd. "Early Development Of Allergic Airways Disease: Do Eosinophils Matter?" 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.a5758.

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Hansbro, Philip M., Ama-Tawiah Essilfie, Jodie L. Simpson, Margaret L. Dunkley, Jay C. Horvat, Peter Gibson, and Paul S. Foster. "Haemophilus Influenzae Induces IL-17-mediated Neutrophilic Allergic Airways Disease." 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.a5603.

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Hansbro, Philip M., Jay C. Horvat, Ama-Tawiah Essilfie, Richard Y. Kim, Jodie L. Simpson, Margaret L. Dunkley, Kenneth W. Beagley, Peter Gibson, and Paul S. Foster. "Infection-Induced Neutrophilic Allergic Airways Disease Is Resistant To Steroid Treatment." 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.a4348.

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Bartlett, N. W., T. Williams, S. L. Loo, and J. Girkin. "IL-25 Inhibits Airway Anti-Viral Immunity and Promotes Virus Exacerbation of Allergic Airways Disease." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1193.

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Hansbro, PM, AN Thorburn, BJ O'Sullivan, R. Thomas, PS Foster, and PG Gibson. "Prevenar Suppresses Allergic Airways Disease through the Induction of Regulatory T Cells." 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.a2228.

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Gray, Kelsey, Judy L. Oakes, Ivana V. Yang, Laura A. Warg, Brian P. O'Connor, and David A. Schwartz. "Dietary Vitamin D Modulates Lung Immunity And Allergic Airways Disease In Mice." 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.a2450.

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Nakada, Emily M., Jichuan Shan, Margaret Kinyanjui, and Elizabeth Fixman. "Alum-dependent Regulation Of Th2/Th17 Responses In Experimental Allergic Airways Disease." 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.a4052.

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Riesenfeld, EP, LK Lundblad, K. O'Neil, C. Protheroe, M. Wu, JH Bates, JJ Lee, NA Lee, and CG Irvin. "Airways Hyperresponsiveness and Major Basic Protein-1 or -2 Deficiency in a Murine Allergic Airways Disease Model." 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.a2441.

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Nakada, Emily M., Jichuan Shan, Margaret W. Kinyanjui, and Elizabeth D. Fixman. "Adjuvant-Dependent Regulation Of IL-17 Production In Murine Experimental Allergic Airways Disease." 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.a1405.

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Crotty Alexander, Laura, Kathryn Akong, and Victor Nizet. "The Role Of Hypoxia Inducible Factor-Alpha Subunits In Allergic Inflammatory Airways Disease." 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.a2575.

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Reports on the topic "Allergic Airways Disease"

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Zhang, Speng, Qinwei Fu, Xin Jin, Junwen Tan, Xinrong Li, and Qinxiu Zhang. Association Between Air Pollution and the Prevalence of Allergic Rhinitis in Chinese Children: Protocol for a Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2021. http://dx.doi.org/10.37766/inplasy2021.10.0094.

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Review question / Objective: For Chinese children, to explore whether air pollution increases the incidence of allergic rhinitis in children. Condition being studied: Allergic rhinitis (AR) is a common chronic inflammatory disease in the upper airways, causing nasal congestion, itching, runny nose, and sneezing. It has serious impacts on people's quality of lives, and affects economic growth indirectly. Epidemiological studies revealed that 10% to 40% of the population were suffering from AR worldwide. In addition, children are more likely to develop allergic rhinitis than adults. The prevalence of allergic rhinitis in children is 25% worldwide, and 4% ~ 31% in China. Eligibility criteria: (1) Trials in which children were AR, and the diagnosis of "AR" was in line with the international guidelines. (2) Children’s age was limited of 0-18 years, and they were born and lived in China and at least one year of exposure to air pollution.(3) Air pollutant concentration in the test was derived from the mean value of data provided by ambient air detectors. (Include NO2, SO2, O3, PM10, PM2.5) (4) Literatures only include cross-sectional studies, cohort and case-control studies. (5) All of these articles provide data that allows us to calculate 95% confidence interval (CI) of the influence of air pollutants on AR. (6) Trials published in English only.
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